115 results on '"Chen, Yan"'
Search Results
2. Prognostic value and microenvironmental crosstalk of exosome-related signatures in human epidermal growth factor receptor 2 positive breast cancer
- Author
-
Zhao Ji, Shen Feng, Hu Yue-Mei, Yin Kai, Chen Ying, Chen Yan-Jie, Hu Qun-Chao, and Liang Li
- Subjects
breast cancer ,exosomes ,human epithelial growth factor receptor 2 ,microenvironment ,prognosis ,biomarkers ,Biology (General) ,QH301-705.5 - Abstract
This study aimed to determine the prognostic value and microenvironmental crosstalk of exosome-related signatures in human epidermal growth factor receptor 2 positive breast cancer (HER2+ BC). Transcriptome sequencing and clinicopathological data were downloaded from the Cancer Genome Atlas. The 10X single cell sequencing dataset was downloaded from the National Center for Biotechnology Information Gene Expression Omnibus. Exosomes-Related Genes were extracted from the ExoCarta and Gene Set Enrichment Analysis databases. FGF9, SF3B4, and EPCAM were found and deemed the most accurate predictive signatures. Patients with HER2+ BC were subtyped into three groupings by exosome prognostic gene (EPGs). The expression of SF3B4 was positively linked with the infiltration of macrophages, neutrophils, and CD4+ T cells. The expression characteristics of EPGs were associated with the biological process of “response to xenobiotic stimuli.” Interactions were relatively high between malignant epithelial cells and fibroblasts, endothelial cells, monocytes, and macrophages. Malignant epithelial cells interact more with fibroblasts and endothelial cells. The migration inhibitory factor pathway was the primary outgoing signaling pattern, while the C-C motif chemokine ligand pathway was the primary incoming signaling pattern for communication between malignant epithelial cells and macrophages. This study described the role of exosome signatures in the prognosis and microenvironment of HER2+ BC and provided a basis for future research.
- Published
- 2024
- Full Text
- View/download PDF
3. RBP7 functions as a tumor suppressor in HR + breast cancer by inhibiting the AKT/SREBP1 pathway and reducing fatty acid
- Author
-
Yu, Yue, Xu, Zhihua, Zhou, Hao, Xu, Ruyan, Xu, Jia, Liu, Wenjun, Wu, Yuxin, Qiu, Yue, Zhang, Guangbo, Huang, Xue, and Chen, Yan
- Published
- 2024
- Full Text
- View/download PDF
4. Rare subclonal sequencing of breast cancers indicates putative metastatic driver mutations are predominately acquired after dissemination
- Author
-
Lawrence-Paul, Matthew R., Pan, Tien-chi, Pant, Dhruv K., Shih, Natalie N. C., Chen, Yan, Belka, George K., Feldman, Michael, DeMichele, Angela, and Chodosh, Lewis A.
- Published
- 2024
- Full Text
- View/download PDF
5. Identification of the prognostic value of Th1/Th2 ratio and a novel prognostic signature in basal-like breast cancer
- Author
-
Xiao, Yu, Huang, Yi, Jiang, Jianping, Chen, Yan, and Wei, Changyuan
- Published
- 2023
- Full Text
- View/download PDF
6. SHMT2 Promotes Invasion and Migration of Breast Cancer Cells Through Binding to and Up-regulating HAX1
- Author
-
CHEN Qianzhi, SHEN Na, ZHANG Ning, and CHEN Yan
- Subjects
breast cancer ,shmt2 ,shmt2 inhibitor ,hax1 ,invasion ,migration ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Objective To explore the molecular mechanism of SHMT2 regulating the invasion and migration of breast cancer cells. Methods Bioinformatics analysis was used to verify the role of SHMT2 in breast cancer tissues. Transwell assay was used to detect the changes of invasion and migration abilities of breast cancer cells. Co-immunoprecipitation, knockdown plasmid transfection and Western blot were used to determine the regulatory relationship between different proteins. Results Bioinformatics analysis showed that the expression level of SHMT2 in invasive breast cancer tissues was significantly higher than that in adjacent normal tissues (P < 0.001). The 5-year disease-specific survival and overall survival in the SHMT2 high expression group were significantly lower than those in the SHMT2 low expression group (both P < 0.001). Transwell assay showed that SHMT2 knockdown significantly reduced the invasion ability (t=5.375, P=0.0058) and migration ability (t=6.274, P=0.0033) of MCF7 cells. Western blot showed that SHMT2 could combine to HAX1, and knockdown of SHMT2 reduced the protein level of HAX1. Transwell assay showed that the inhibitory effect of SHMT2 knockdown on the migration of MCF7 cells could be reversed by overexpression of HAX1 (t=6.274, P=0.0033; t=8.041, P=0.0013), while SHMT2 inhibitor (SHIN1, 10 nmol/L) significantly inhibited the migration of MCF7 cells induced by SHMT2 overexpression (t=10.16, P=0.0005; t=8.741, P=0.0009). Conclusion SHMT2 was closely related to the poor prognosis of breast cancer, and was a key factor in the invasion and migration of breast cancer cells. The mechanism was that SHMT2 increased the invasion and migration ability of breast cancer cells by binding to and up-regulating HAX1. It was verified that SHMT2 inhibitor could significantly reduce the migration ability of breast cancer cells. This study explored the therapeutic potential of SHMT2 inhibitor in metastatic breast cancer, and found potential intervention targets for its clinical treatment.
- Published
- 2023
- Full Text
- View/download PDF
7. Expression and clinical implications of basic leucine zipper ATF-like transcription factor 2 in breast cancer
- Author
-
Lin, Yingying, Zhou, Xusheng, Peng, Wei, Wu, Jing, Wu, Xiufeng, Chen, Yan, and Cui, Zhaolei
- Published
- 2021
- Full Text
- View/download PDF
8. Causal effects of genetically predicted endometriosis on breast cancer: a two-sample Mendelian randomization study.
- Author
-
Yan, Shuixin, Li, Jiadi, Chen, Jiafeng, Chen, Yan, Qiu, Yu, Zhou, Yuxin, and Wu, Weizhu
- Subjects
BREAST cancer ,ENDOMETRIOSIS ,DISEASE risk factors ,ESTROGEN receptors ,CANCER invasiveness ,BREAST ,ODDS ratio - Abstract
This study used a Mendelian randomization (MR) approach to investigate the causal relationship between genetically predicted endometriosis (EMS) and breast cancer risk. A total of 122,977 cases and 105,974 controls were included in the analysis, with gene-level summary data obtained from the Breast Cancer Association Consortium (BCAC). An inverse variance-weighting approach was applied to assess the causal relationship between EMS and breast cancer risk, and weighted median and MR-Egger regression methods were used to evaluate pleiotropy. Results showed a causal relationship between EMS and a decreased risk of overall breast cancer (odds ratio [OR] 0.95; 95% CI 0.90–0.99, p = 0.02). Furthermore, EMS was associated with a lower risk for estrogen receptor (ER)-positive breast cancer in a subgroup analysis based on immunohistochemistry type (OR 0.91; 95% CI 0.86–0.97, p = 0.005). However, there was no causal association between ER-negative breast cancer and survival (OR 1.00; 95% CI 0.94–1.06, p = 0.89). Pleiotropy was not observed. These findings provide evidence of a relationship between EMS and reduced breast cancer risk in invasive breast cancer overall and specific tissue types, and support the results of a previous observational study. Further research is needed to elucidate the mechanisms underlying this association. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
9. Shugan Liangxue Decoction (舒肝凉血方) Down-Regulates Estrogen Receptor α Expression in Breast Cancer Cells
- Author
-
Zhou, Ning, Han, Shu-yan, Chen, Yan-zhi, Zhou, Fei, Zheng, Wen-xian, and Li, Ping-ping
- Published
- 2018
- Full Text
- View/download PDF
10. Advantages with prophylactic PEG-rhG-CSF versus rhG-CSF in breast cancer patients receiving multiple cycles of myelosuppressive chemotherapy: an open-label, randomized, multicenter phase III study
- Author
-
Xie, Jie, Cao, Jun, Wang, Jing-fen, Zhang, Bai-hong, Zeng, Xiao-hua, Zheng, Hong, Zhang, Yang, Cai, Li, Wu, Yu-dong, Yao, Qiang, Zhao, Xiao-chun, Mao, Wei-dong, Jiang, Ai-Mei, Chen, Shao-shui, Yang, Shun-e, Wang, Shu-sen, Wang, Jian-hong, Pan, Yue-yin, Ren, Bi-yong, Chen, Yan-ju, Ouyang, Li-zhi, Lei, Kai-jian, Gao, Jing-hua, Huang, Wen-he, Huang, Zhan, Shou, Tao, He, Yan-ling, Cheng, Jing, Sun, Yang, Li, Wei-ming, Cui, Shu-de, Wang, Xin, Rao, Zhi-guo, Ma, Hu, Liu, Wei, Wu, Xue-yong, Shen, Wei-xi, Cao, Fei-lin, Xiao, Ze-min, Wu, Biao, Tian, Shu-yan, Meng, Dong, Shen, Peng, Wang, Bi-yun, Wang, Zhonghua, Zhang, Jian, Wang, Leiping, and Hu, Xi-chun
- Published
- 2018
- Full Text
- View/download PDF
11. Improved Differential Diagnosis Based on BI-RADS Descriptors and Apparent Diffusion Coefficient for Breast Lesions: A Multiparametric MRI Analysis as Compared to Kaiser Score.
- Author
-
Meng, Lingsong, Zhao, Xin, Guo, Jinxia, Lu, Lin, Cheng, Meiying, Xing, Qingna, Shang, Honglei, Zhang, Bohao, Chen, Yan, Zhang, Penghua, and Zhang, Xiaoan
- Abstract
To develop the nomogram utilizing the American College of Radiology BI-RADS descriptors, clinical features, and apparent diffusion coefficient (ADC) to differentiate benign from malignant breast lesions. A total of 341 lesions (161 malignant and 180 benign) were included. Clinical data and imaging features were reviewed. Univariable and multivariable logistic regression analyses were performed to determine the independent variables. ADC as a continuous or classified into binary form with a cutoff value of 1.30 × 10
−3 mm2 /s, incorporated other independent predictors to construct two nomograms, respectively. Receiver operating curve and calibration plot was employed to test the models' discriminative ability. The diagnostic performance between the developed model and the Kaiser score (KS) was also compared. In both models, high patient age, the presence of root sign, time-intensity curves (TICs) types (plateau and washout), heterogenous internal enhancement, the presence of peritumoral edema, and ADC were independently associated with malignancy. The AUCs of two multivariable models (AUC, 0.957; 95% CI: 0.929–0.976 and AUC, 0.958; 95% CI: 0.931–0.976) were significantly higher than that of the KS (AUC, 0.919, 95% CI: 0.885–0.946; both P < 0.001). At the same sensitivity of 95.7%, our models showed an increase in specificity by 5.56% (P = 0.076) and 6.11% (P = 0.035), respectively, as compared to the KS. The models incorporating MRI features (root sign, TIC, margins, internal enhancement, and presence of edema), quantitative ADC value, and patient age showed improved diagnostic performance and might have avoided more unnecessary biopsies in comparison with the KS, although further external validation is required. [ABSTRACT FROM AUTHOR]- Published
- 2023
- Full Text
- View/download PDF
12. Performance of a PLK1‐based immune risk model for prognosis and treatment response prediction in breast cancer.
- Author
-
Chen, Yan, You, Yiqing, Wu, Qiaoling, Wu, Jing, Lin, Shujing, Sun, Yang, and Cui, Zhaolei
- Subjects
- *
PACLITAXEL , *REGULATORY T cells , *GENE expression , *B cell receptors , *T cell receptors , *BREAST cancer , *IMMUNE checkpoint proteins - Abstract
Objective: Polo‐like kinase 1 (PLK1), a serine/threonine‐protein kinase, functions as a potent oncogene in the initiation and progression of tumor. The aim of this study is to assess potential correlations between PLK1 expression and immune infiltration in breast cancer (BRCA) and construct a PLK1‐based immune risk model applicable for prognosis and treatment response prediction in BRCA. Methods: We collected data on PLK1 gene expression in BRCA patients from The Cancer Genome Atlas (TCGA) database. Thereafter, we analyzed the associations of PLK1 expression with immune cell infiltration and immunomodulators, and established a prognostic risk model based on seven PLK1‐associated immunomodulator genes and a nomogram for survival prediction. Results: BRCA prognosis, clinical stage progression, and tumor classification were all shown to be substantially correlated with PLK1 expression. The PLK1 gene was significantly enriched in T cell and B cell receptors and molecules of the chemokine signaling pathways. Specifically, PLK1 expression was positively correlated with the CD8+ T cell and regulatory T cell (Tregs) activation and negatively correlated with M2 macrophage infiltration. The seven‐genes‐based risk model could serve as an independent prognostic factor of BRCA. The risk model was markedly correlated with the expression of programmed cell death protein 1/programmed cell death ligand 1 (PD‐1/PD‐L1; both p < 0.001) immune checkpoints, and tumor mutation burden (TMB). High‐ and low‐risk BRCA patients identified by the risk model responded differently to anti‐PD‐1 and/or anti‐CTLA4 therapy, as well as common chemotherapy drugs, like cisplatin, paclitaxel, and gemcitabine. Conclusion: This PLK1‐based immune risk model can effectively predict the prognosis and tumor progression of BRCA, identify gene mutations, and evaluate patient's response toward immunotherapy and chemotherapy regimens. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
13. Survival and disease-free benefits with mastectomy versus breast conservation therapy for early breast cancer: a meta-analysis
- Author
-
Chen, Yan, Jiang, Lei, Gao, Bo, Cheng, Zhi-yuan, Jin, Jiaxin, and Yang, Ke-hu
- Published
- 2016
- Full Text
- View/download PDF
14. Ginger-Derived 3HDT Exerts Antiproliferative Effects on Breast Cancer Cells by Apoptosis and DNA Damage.
- Author
-
Chen, Chung-Yi, Chen, Yan-Ning, Shiau, Jun-Ping, Tang, Jen-Yang, Hou, Ming-Feng, and Chang, Hsueh-Wei
- Subjects
- *
BREAST cancer , *CANCER cells , *TRIPLE-negative breast cancer , *DRUG efficacy , *REACTIVE oxygen species , *GLUTATHIONE - Abstract
Ginger-derived compounds are abundant sources of anticancer natural products. However, the anticancer effects of (E)-3-hydroxy-1-(4′-hydroxy-3′,5′-dimethoxyphenyl)-tetradecan-6-en-5-one (3HDT) have not been examined. This study aims to assess the antiproliferation ability of 3HDT on triple-negative breast cancer (TNBC) cells. 3HDT showed dose-responsive antiproliferation for TNBC cells (HCC1937 and Hs578T). Moreover, 3HDT exerted higher antiproliferation and apoptosis on TNBC cells than on normal cells (H184B5F5/M10). By examining reactive oxygen species, mitochondrial membrane potential, and glutathione, we found that 3HDT provided higher inductions for oxidative stress in TNBC cells compared with normal cells. Antiproliferation, oxidative stress, antioxidant signaling, and apoptosis were recovered by N-acetylcysteine, indicating that 3HDT preferentially induced oxidative-stress-mediated antiproliferation in TNBC cells but not in normal cells. Moreover, by examining γH2A histone family member X (γH2AX) and 8-hydroxy-2-deoxyguanosine, we found that 3HDT provided higher inductions for DNA damage, which was also reverted by N-acetylcysteine. In conclusion, 3HDT is an effective anticancer drug with preferential antiproliferation, oxidative stress, apoptosis, and DNA damage effects on TNBC cells. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
15. Construction of a lncRNA-mediated ceRNA network and a genomic-clinicopathologic nomogram to predict survival for breast cancer patients.
- Author
-
Wu, Mengni, Lu, Linlin, Dai, Tiantian, Li, Aoshuang, Yu, Yue, Li, Yadi, Xu, Zhihua, and Chen, Yan
- Subjects
NOMOGRAPHY (Mathematics) ,CANCER patients ,DISEASE risk factors ,BREAST cancer ,PROGNOSTIC models - Abstract
Breast cancer (BC) is the most common cancer among women and a leading cause of cancer-related deaths worldwide. The diagnosis of early patients and the prognosis of advanced patients have not improved over the past several decades. The purpose of the present study was to identify the lncRNA-related genes based on ceRNA network and construct a credible model for prognosis in BC. Based on The Cancer Genome Atlas (TCGA) database, prognosis-related differently expressed genes (DEGs) and a lncRNA-associated ceRNA regulatory network were obtained in BC. The patients were randomly divided into a training group and a testing group. A ceRNA-related prognostic model as well as a nomogram was constructed for further study. A total of 844 DElncRNAs, 206 DEmiRNAs and 3295 DEmRNAs were extracted in BC, and 12 RNAs (HOTAIR, AC055854.1, ST8SIA6-AS1, AC105999.2, hsa-miR-1258, hsa-miR-7705, hsa-miR-3662, hsa-miR-4501, CCNB1, UHRF1, SPC24 and SHCBP1) among them were recognized for the construction of a prognostic risk model. Patients were then assigned to high-risk and low-risk groups according to the risk score. The Kaplan-Meier (K-M) analysis demonstrated that the high-risk group was closely associated with poor prognosis. The predictive nomogram combined with clinical features showed performance in clinical practice. In a nutshell, our ceRNA-related gene model and the nomogram graph are accurate and reliable tools for predicting prognostic outcomes of BC patients, and may make great contributions to modern precise medicine. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
16. Effects of Decabrominated Diphenyl Ether (PBDE-209) in Regulation of Growth and Apoptosis of Breast, Ovarian, and Cervical Cancer Cells
- Author
-
Li, Zhi-Hua, Liu, Xiao-Yan, Wang, Na, Chen, Jing-Si, Chen, Yan-Hong, Huang, Jin-Tao, Su, Chun-Hong, Xie, Fukang, Yu, Bin, and Chen, Dun-Jin
- Published
- 2012
17. Oroxylin A suppresses breast cancer-induced osteoclastogenesis and osteolysis as a natural RON inhibitor.
- Author
-
Chen, Yan, Zheng, Jiehuang, Mo, Lixia, Chen, Fengsheng, Li, Ruopeng, Wang, Yiyuan, Liang, Qinghe, Chen, Ziye, Dai, Wenqi, Chen, Lishan, Yan, Peiyu, Zhou, Hua, and Li, Xiaojuan
- Abstract
Malignant breast cancer cells trigger the over-activation of osteoclast precursor cells, leading to bone loss and severe pain. Targeted inhibition of osteoclast differentiation has emerged as an important strategy for treating bone syndromes induced by breast cancer. The objective is to discover natural osteoclast inhibitor to treat osteoclastogenesis and bone destruction induced by breast cancer, and clarify the specific mechanisms. Recepteur d'origine Nantais (RON) protein was employed to search the natural osteoclast inhibitor for breast cancer-induced osteoclastogenesis by molecular docking, molecular dynamics simulation and cellular thermal shift assay (CETSA). In the in vitro experiment, breast cancer MDA-MB-231 cell-conditioned medium (MDA-MB-231 CM) was used to induce osteoclastogenesis in murine bone marrow-derived macrophages (BMMs), aiming to elucidate the effects and mechanisms of the natural osteoclast inhibitor. In the in vivo model, MDA-MB-231 cells was injected into the mouse tibia to evaluate the therapeutic effect of drug on breast cancer-induced bone destruction. We discovered a significant increase in the expression of RON during MDA-MB-231 CM-induced osteoclast differentiation in vitro. Molecular docking analysis found that oroxylin A (OA), a flavonoid derived from the Chinese medicine Scutellaria baicalensis Georgi , showed binding ability with RON, while its impact and mechanism on breast cancer-induced osteoclastogenesis and osteolysis remains unclear. Molecular dynamics simulation and CETSA further revealed that OA bound directly to the RON protein, and it also decreased RON expression in breast cancer CM-induced osteoclastogenesis. Correspondingly, OA suppressed the MDA-MB-231 CM-induced osteoclastogenesis and bone resorption in vitro. The downstream signals of RON including Src and NFATc1, as well as the osteoclast-specific genes, were downregulated by OA. Of interesting, the suppressive effect of OA on osteoclastogenesis induced by MDA-MB-231 CM was abolished after RON was knocked down by the specific RON-siRNA, this further confirmed that OA showed inhibitory effects on osteoclasts through targeting RON. In addition, we found that OA attenuated MDA-MB-231 cell-induced osteolysis and reduced the number of osteoclasts in vivo. Our results indicate that OA acts as a natural RON inhibitor to suppress breast cancer-induced osteoclastogenesis and osteolysis. This provides new strategy for treating breast cancer-induced bone destruction and related syndromes. [Display omitted] [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
18. miR-506-loaded gelatin nanospheres target PENK and inactivate the ERK/Fos signaling pathway to suppress triple-negative breast cancer aggressiveness
- Author
-
Jie Liu, Wei-Hong Guo, Ge Zhang, Shi-Long Zhang, Jing-Bao Li, Wen-Jing Liu, Qiang Chen, Da-Chuan Yin, Chang-Qing Yang, Chen-Yan Zhang, Xin-Li Liu, and Gang Zhao
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Cancer Research ,Triple Negative Breast Neoplasms ,Biology ,Metastasis ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Breast cancer ,In vivo ,Cell Line, Tumor ,microRNA ,medicine ,Animals ,Humans ,Viability assay ,Protein Precursors ,Extracellular Signal-Regulated MAP Kinases ,Molecular Biology ,Triple-negative breast cancer ,Gene Transfer Techniques ,Enkephalins ,medicine.disease ,Xenograft Model Antitumor Assays ,Gene Expression Regulation, Neoplastic ,Disease Models, Animal ,MicroRNAs ,030104 developmental biology ,030220 oncology & carcinogenesis ,Cancer research ,Disease Progression ,Gelatin ,Female ,Signal transduction ,Proto-Oncogene Proteins c-fos ,Nanospheres ,Signal Transduction - Abstract
Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer. Some microRNAs (miRNAs) were abnormally expressed in TNBC, and they are closely related to the occurrence and progression of TNBC. Here, we found that miR-506 was significantly downregulated in TNBC and relatively lower miR-506 expression predicted a poorer prognosis. Moreover, we found that miR-506 could inhibit MDA-MB-231 cell viability, colony formation, migration, and invasion, and suppress the ERK/Fos oncogenic signaling pathway through upregulating its direct target protein proenkephalin (PENK). Therefore, miR-506 was proposed as a nucleic acid drug for TNBC therapy. However, miRNA is unstable in vivo, which limiting its application as a therapeutic drug via conventional oral or injected therapies. Here, a gelatin nanosphere (GN) delivery system was applied for the first time to load exogenous miRNA. Exogenous miR-506 mimic was loaded on GNs and injected into the in situ TNBC animal model, and the miR-506 could achieve sustained and controlled release. The results confirmed that overexpression of miR-506 and PENK in vivo through loading on GNs inhibited in situ triple-negative breast tumor growth and metastasis significantly in the xenograft model. Moreover, we indicated that the ERK/Fos signaling pathway was intensively inactivated after overexpression of miR-506 and PENK both in vitro and in vivo, which was further validated by the ERK1/2-specific inhibitor SCH772984. In conclusion, this study demonstrates that miR-506-loaded GNs have great potential in anti-TNBC aggressiveness therapy.
- Published
- 2021
19. Progress of non-coding RNAs in triple-negative breast cancer
- Author
-
Ge Zhang, Da-Chuan Yin, Jie Liu, Zhao Shiqi, Li-Heng Luo, Xin-Li Liu, Chen-Yan Zhang, Gang Zhao, and Shi-Long Zhang
- Subjects
0301 basic medicine ,RNA, Untranslated ,Cell ,Triple Negative Breast Neoplasms ,Biology ,030226 pharmacology & pharmacy ,General Biochemistry, Genetics and Molecular Biology ,Chromatin remodeling ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,microRNA ,medicine ,Biomarkers, Tumor ,Humans ,General Pharmacology, Toxicology and Pharmaceutics ,Triple-negative breast cancer ,General Medicine ,RNA, Circular ,Cell cycle ,medicine.disease ,Non-coding RNA ,Prognosis ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,030104 developmental biology ,medicine.anatomical_structure ,Cancer research ,Female ,RNA, Long Noncoding ,Transcriptome - Abstract
Non-coding RNAs (ncRNAs) include miRNA, lncRNA, and circRNA. NcRNAs are involved in multiple biological processes, including chromatin remodeling, signal transduction, post-transcriptional modification, cell autophagy, carbohydrate metabolism, and cell cycle regulation. Triple negative breast cancer (TNBC) is notorious for high invasiveness and metastasis, poor prognosis, and high mortality, and it is the most malignant breast cancer, while the effective targets for TNBC treatment are still lacking. NcRNAs act as oncogenes or suppressor genes, as well as promote or inhibit the occurrence and development of TNBC. Here, we reviewed some important miRNAs, lncRNAs, circRNAs, their target(s) and molecular mechanisms in TNBC. It is benefited to understand the occurrence and development of TNBC, further some ncRNAs might be potential targets for TNBC treatment.
- Published
- 2020
20. Risk Factors of Brain Metastasis and Prognosis in HER2-Positive Breast Cancer: A Single-Institution Retrospective Analysis from China.
- Author
-
Cai, Shuang-Long, Wang, Zhi-Hong, Chen, Xiao-Geng, Han, Lei, Gong, Guo-Xian, Chen, Yan-Ping, Lin, Xiu-Quan, Ma, Tao, and Chen, Hong-Dan
- Subjects
HER2 positive breast cancer ,BREAST cancer prognosis ,BRAIN metastasis ,LOGISTIC regression analysis ,FISHER exact test ,HORMONE receptor positive breast cancer - Abstract
Background: Brain metastasis (BM) frequently occurs in HER2-positive breast cancer (BC) patients, but the risk factors of BM in this type of patients are still unknown. Our study aims to assess the risk factors of BM and prognostic analysis in HER2-positive BC patients. Methods: Univariate analysis used t -test, chi-square test, and Fisher's exact test to find out the risk factors for BM, and multivariable analysis was done with stepwise logistic regression analysis. Prognostic data analysis was estimated by the Kaplan–Meier method. Results: A total of 228 HER2-positive BC patients were included, of whom 214 patients were postoperative metastatic patients and 14 patients were de novo stage IV patients. Through comparing the stratified variables between 51 postoperative metastatic patients with BM and 163 postoperative metastatic patients without BM, the multivariate analysis showed that age ≤40 years (OR 2.321, 95% CI: 1.089 to 4.948) and first metastatic site with lung metastasis (OR 2.168, 95% CI: 1.099 to 4.274) were independent risk factors for BM in HER2-positive BC patients. Prognostic data of all 65 HER2-positive BC patients with BM showed that the time from the diagnosis of BC to the development of breast cancer brain metastasis (BCBM) was 36.3 months (95% CI: 30.0 to 42.1 months). The time from the diagnosis of first recurrence and metastasis stage to the diagnosis of BCBM was 11.35 months (95% CI: 7.1 to 18.4 months). The time from the diagnosis of BCBM to the time of follow-up was 24.1 months (95% CI: 13.9 to 37.5 months). Up until the time of follow-up data, a total of 38 patients had died, and the time from the diagnosis of BM of these 38 patients to death was 11.0 months (95% CI: 9.0 to 20.4 months). Conclusion: The prognosis of HER2-positive BC patients with BM was poor due to the lack of effective treatments for BM. Age ≤40 years and first metastatic site with lung metastasis were the independent risk factors for BM in HER2-positive BC patients. Future research about pre-emptive medical interventions may help to improve the prognosis of HER2-positive BC patients with high risk to develop BM. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
21. USP5 promotes breast cancer cell proliferation and metastasis by stabilizing HIF2α.
- Author
-
Huang, Weixiao, Liu, Xiong, Zhang, Yao, Deng, Mingxia, Li, Guangqiang, Chen, Guo, Yu, Li, Jin, Lai, Liu, Tongzheng, Wang, Yijie, and Chen, Yan
- Subjects
CANCER cells ,CANCER cell proliferation ,BREAST cancer ,DEUBIQUITINATING enzymes ,HYPOXIA-inducible factors ,PROTEIN stability - Abstract
Hypoxia‐inducible factor 2α (HIF2α) plays a pivotal role in breast tumor growth and metastasis. However, the regulatory mechanisms of HIF2α protein stability remain poorly understood. The precise role of the deubiquitinase (DUB) ubiquitin‐specific peptidase 5 (USP5) in breast cancer and the underlying mechanism remains largely unknown. Here, we identified USP5 as a novel DUB for HIF2α. Physically, USP5 interacts with HIF2α and protects HIF2α from ubiquitin‐proteasome degradation, thereby promoting the transcription of HIF2α target genes, such as SLC2A1, PLOD2, P4HA1, and VEGFA. USP5 ablation impairs breast cancer cells proliferation, colony formation, migration, and invasion. Moreover, USP5 is highly expressed in breast cancer, and the protein levels of USP5 are positively correlated with HIF2α protein levels in human breast cancer tissues. Importantly, high levels of USP5 leads to poor clinical outcome in patients with breast cancer. Collectively, USP5 stabilizes HIF2α through its DUB activity and provides a potential therapeutic target for breast cancer. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
22. Role of TG2 and TGF-β1 in the pathogenesis of human breast cancer
- Author
-
Gao, Hai-Cheng, Huang, Yan-Zhi, Liu, Yu-Qi, Chen, Yan, Wang, Zhe-Hui, and Yin, Guang-Hao
- Subjects
breast cancer ,cell death ,tissue transaminase ,cisplatin ,Articles ,skin and connective tissue diseases ,transforming growth factor-β1 - Abstract
The present study analyzed the role of transforming growth factor-β1 (TGF-β1) and tissue transglutaminase (TG2) in breast cancer, as well as their protein levels in MCF-7 cells treated with cisplatin. In addition, the present study investigated the effects of TG2 and TGF-β1 in MCF-7 cells following TGF-β1 and TG2 inhibition or TGF-β1 induction. The protein levels of TG2 and TGF-β1 in breast cancer tissues and in MCF-7 cells treated with cisplatin, TG2 and TGF-β1 inhibitors or 10 ng/ml TGF-β1 were analyzed by immunohistochemical staining, immunofluorescence and western blotting. The results revealed that the expression levels of TG2 and TGF-β1 in breast cancer tissues were significantly higher compared with those in paracancerous tissues. The fluorescence intensity of TG2 and TGF-β1 in MCF-7 cells treated with cisplatin was lower compared with that in untreated MCF-7 cells. Using bioinformatics analysis, the present study predicted that TGF-β1 may be associated with TG2. In addition, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with inhibitors of TGF-β1 and TG2 were lower compared with those in untreated MCF-7 cells. By contrast, the expression levels of TGF-β1 and TG2 in MCF-7 cells treated with TGF-β1 were higher compared with those in untreated MCF-7 cells. Therefore, the present study demonstrated that TGF-β1 and TG2 may serve an important role in breast cancer tissues and in MCF-7 cells. In addition, it was revealed that TG2 and TGF-β1 may have a synergistic role in MCF-7 cells.
- Published
- 2020
23. Identification of blood protein biomarkers for breast cancer staging by integrative transcriptome and proteome analyses
- Author
-
Chen Yan, Yan Zhang, Fang Yao, Jiazuan Ni, Dongxian Zhou, and Liming Shen
- Subjects
0301 basic medicine ,Proteomics ,Proteome ,Biophysics ,Breast Neoplasms ,Disease ,Computational biology ,Biology ,Malignancy ,Biochemistry ,Transcriptome ,03 medical and health sciences ,Breast cancer ,medicine ,Biomarkers, Tumor ,Humans ,skin and connective tissue diseases ,Gene ,Neoplasm Staging ,030102 biochemistry & molecular biology ,Blood Proteins ,medicine.disease ,Blood proteins ,030104 developmental biology ,Biomarker (medicine) ,Female - Abstract
Breast cancer is the most common malignancy for women. Accurate prediction of breast cancer and its pathological stages is important for treatment decision-making. Although many studies have focused on discovering circulating biomarkers of breast cancer, no such biomarkers have been reported for different stages of this disease. In this study, we identified blood protein biomarkers for each stage of breast cancer by analyzing transcriptome and proteome data from patients. Analysis of the TCGA transcriptome datasets revealed that a large number of genes were differentially expressed in tumor samples of each stage of breast cancer compared with adjacent normal tissues. Blood-secretory proteins encoded by these genes were then predicted by bioinformatics programs. Furthermore, iTRAQ-based proteomic analysis was conducted for plasma samples of breast cancer patients with different stages. A portion of predicted blood-secretory proteins could be detected and verified differentially expressed. Finally, several proteins were chosen as potential blood protein biomarkers for different stages of breast cancer due to their consistent expression patterns at both mRNA and protein levels. Overall, our data provide new insights into diagnosis and classification of breast cancer as well as selection of optimal treatments. SIGNIFICANCE: We identified blood protein biomarkers for each stage of breast cancer by analyzing tissue-based transcriptome and blood-based proteome data from patients. To our knowledge, this is the first time to try to identify blood protein biomarkers for different stages of breast cancer via these integrative analyses. Our data may provide new insights into diagnosis and classification of breast cancer as well as selection of optimal treatment.
- Published
- 2020
24. Comparison of comfort and complications of Implantable Venous Access Port (IVAP) with ultrasound guided Internal Jugular Vein (IJV) and Axillary Vein/Subclavian Vein (AxV/SCV) puncture in breast cancer patients: a randomized controlled study.
- Author
-
Chen, Yan Bo, Bao, Hao Shi, Hu, Ting Ting, He, Zhou, Wen, Biaolin, Liu, Feng Tao, Su, Feng Xi, Deng, He Ran, and Wu, Jian Nan
- Subjects
- *
SUBCLAVIAN veins , *JUGULAR vein , *CANCER patients , *BREAST cancer , *CENTRAL venous catheters , *ARTERIAL catheters , *ARTERIAL puncture - Abstract
Background: Axillary vein/subclavian vein (AxV/SCV) and Internal jugular vein (IJV) are commonly used for implantable venous access port (IVAP) implantation in breast cancer patients for chemotherapy. Previous research focused on comparison of complications while patient comfort was ignored. This study aims to compare patient comfort, surgery duration and complications of IVAP implantation between IJV and AxV/SCV approaches.Methods: Two hundred forty-eight breast cancer patients were enrolled in this randomized controlled study from August 2020 to June 2021. Patients scheduled to undergo IVAP implantation were randomly and equally assigned to receive central venous catheters with either AxV /SCV or IJV approaches. All patients received comfort assessment using a comfort scale table at day 1, day 2 and day 7 after implantation. Patient comfort, procedure time of operation as well as early complications were compared.Results: Patient comfort was significantly better in the AxV/SCV group than that of IJV group in day 1 (P < 0.001), day 2 (P < 0.001) and day 7(P = 0.023). Procedure duration in AxV/SCV group was slightly but significantly shorter than IJV group (27.14 ± 3.29 mins vs 28.92 ± 2.54 mins, P < 0.001). More early complications occurred in AxV/SCV group than IJV group (11/124 vs 2/124, P = 0.019). No difference of complications of artery puncture, pneumothorax or subcutaneous hematoma between these two groups but significantly more catheter misplacement in AxV/SCV group than IJV group (6/124 vs 0/124, P = 0.029). Absolutely total risk of complications was rather low in both groups (8.87% in AxV/SCV group and 1.61% in IJV group).Conclusions: Our study indicates that patients with AxV/SCV puncture have higher comfort levels than IJV puncture. AxV/SCV puncture has shorter procedure duration but higher risk of early complications, especially catheter misplacement. Both these two approaches have rather low risk of complications. Consequently, our study provides an alternative choice for breast cancer patients to reach better comfort. [ABSTRACT FROM AUTHOR]- Published
- 2022
- Full Text
- View/download PDF
25. PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
- Author
-
Yunde Liu, Qingjuan Yao, Weiwei Kong, Yaqing Chen, Liya Fu, Chen Yan, and Yuhua Yuan
- Subjects
0301 basic medicine ,Cancer Research ,medicine.drug_class ,Carcinogenesis ,Breast Neoplasms ,Biology ,Cell Line ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,Cell Movement ,Cell Line, Tumor ,microRNA ,medicine ,Humans ,Breast ,PVT1 ,STAT6 ,Cell growth ,Cell Cycle ,miR‐1207‐5p ,General Medicine ,Original Articles ,Cell cycle ,Middle Aged ,medicine.disease ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,030104 developmental biology ,cell proliferation ,Cell Transformation, Neoplastic ,HEK293 Cells ,Oncology ,Estrogen ,030220 oncology & carcinogenesis ,Cancer research ,Ectopic expression ,Original Article ,RNA, Long Noncoding ,CDKN1B ,STAT6 Transcription Factor - Abstract
Accumulating evidence indicates that ectopic expression of non-coding RNAs are responsible for breast cancer progression. Increased non-coding RNA PVT1, the host gene of microRNA-1207-5p (miR-1207-5p), has been associated with breast cancer proliferation. However, how PVT1 functions in breast cancer is still not clear. In this study, we show a PVT1-derived microRNA, miR-1207-5p, that promotes the proliferation of breast cancer cells by directly regulating STAT6. We first confirm the positive correlated expression pattern between PVT1 and miR-1207-5p by observing consistent induced expression by estrogen, and overexpression in breast cancer cell lines and breast cancer patient specimens. Moreover, silence of PVT1 also decreased miR-1207-5p expression. Furthermore, increased miR-1207-5p expression promoted, while decreased miR-1207-5p expression suppressed, cell proliferation, colony formation, and cell cycle progression in breast cancer cell lines. Mechanistically, a novel target of miR-1207-5p, STAT6, was identified by a luciferase reporter assay. Overexpression of miR-1207-5p decreased the levels of STAT6, which activated CDKN1A and CDKN1B to regulate the cell cycle. We also confirmed the reverse correlation of miR-1207-5p and STAT6 expression levels in breast cancer samples. Therefore, our findings reveal that PVT1-derived miR-1207-5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression. These findings suggest miR-1207-5p might be a potential target for breast cancer therapy.
- Published
- 2017
26. A Comparative Assessment of MR BI-RADS 4 Breast Lesions With Kaiser Score and Apparent Diffusion Coefficient Value.
- Author
-
Meng, Lingsong, Zhao, Xin, Lu, Lin, Xing, Qingna, Wang, Kaiyu, Guo, Yafei, Shang, Honglei, Chen, Yan, Huang, Mengyue, Sun, Yongbing, and Zhang, Xiaoan
- Subjects
DIFFUSION coefficients ,CANCER diagnosis ,RECEIVER operating characteristic curves ,SENSITIVITY & specificity (Statistics) ,BREAST imaging - Abstract
Objectives: To investigate the diagnostic performance of the Kaiser score and apparent diffusion coefficient (ADC) to differentiate Breast Imaging Reporting and Data System (BI-RADS) Category 4 lesions at dynamic contrast-enhanced (DCE) MRI. Methods: This was a single-institution retrospective study of patients who underwent breast MRI from March 2020 to June 2021. All image data were acquired with a 3-T MRI system. Kaiser score of each lesion was assigned by an experienced breast radiologist. Kaiser score+ was determined by combining ADC and Kaiser score. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic performance of Kaiser score+, Kaiser score, and ADC. The area under the curve (AUC) values were calculated and compared by using the Delong test. The differences in sensitivity and specificity between different indicators were determined by the McNemar test. Results: The study involved 243 women (mean age, 43.1 years; age range, 18–67 years) with 268 MR BI-RADS 4 lesions. Overall diagnostic performance for Kaiser score (AUC, 0.902) was significantly higher than for ADC (AUC, 0.81; p = 0.004). There were no significant differences in AUCs between Kaiser score and Kaiser score+ (p = 0.134). The Kaiser score was superior to ADC in avoiding unnecessary biopsies (p < 0.001). Compared with the Kaiser score alone, the specificity of Kaiser score+ increased by 7.82%, however, at the price of a lower sensitivity. Conclusion: For MR BI-RADS category 4 breast lesions, the Kaiser score was superior to ADC mapping regarding the potential to avoid unnecessary biopsies. However, the combination of both indicators did not significantly contribute to breast cancer diagnosis of this subgroup. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
27. Baicalein resensitizes tamoxifen‐resistant breast cancer cells by reducing aerobic glycolysis and reversing mitochondrial dysfunction via inhibition of hypoxia‐inducible factor‐1α.
- Author
-
Chen, Yan, Zhang, Jingyu, Zhang, Minqin, Song, Yuxuan, Zhang, Yue, Fan, Shuangqin, Ren, Shuang, Fu, Lingyun, Zhang, Nenling, Hui, Hui, and Shen, Xiangchun
- Subjects
- *
BREAST cancer , *CANCER cells , *GLYCOLYSIS , *MITOCHONDRIAL DNA , *MITOCHONDRIA , *MONOCARBOXYLATE transporters , *REACTIVE oxygen species , *LACTATION - Abstract
Drug resistance is a major hurdle for the effectiveness of tamoxifen (TAM) to provide clinical benefit. Therefore, it is essential to identify a sensitizer that could be used to improve TAM efficacy in treating TAM‐resistant breast cancer. Here, we investigated the ability of baicalein to reverse TAM resistance. We found that baicalein increased the efficacy of TAM in inhibiting proliferation and inducing apoptosis of TAM‐resistant cells. It also enhanced the TAM‐induced growth reduction of resistant cells from NOD/SCID mouse mammary fat pads, without causing obvious systemic toxicity. Analyses using the CellMiner tool and the Kaplan–Meier plotter database showed that HIF‐1α expression was inversely correlated with TAM therapeutic response in NCI‐60 cancer cells and breast cancer patients. HIF‐1α expression was increased in TAM‐resistant cells due to an increase in mRNA levels and reduced ubiquitin‐mediated degradation. Baicalein reduced HIF‐1α expression by promoting its interaction with PHD2 and pVHL, thus facilitating ubiquitin ligase‐mediated proteasomal degradation and thereby suppressing the nuclear translocation, binding to the hypoxia‐response element, and transcriptional activity of HIF‐1α. As a result, baicalein downregulated aerobic glycolysis by restricting glucose uptake, lactate production, ATP generation, lactate/pyruvate ratio and expression of HIF‐1α‐targeted glycolytic genes, thereby enhancing the antiproliferative efficacy of TAM. Furthermore, baicalein interfered with HIF‐1α inhibition of mitochondrial biosynthesis, which increased mitochondrial DNA content and mitochondrial numbers, restored the generation of reactive oxygen species in mitochondria, and thus enhanced the TAM‐induced mitochondrial apoptotic pathway. The HIF‐1α stabilizer dimethyloxallyl glycine prevented the baicalein‐induced downregulation of glycolysis and mitochondrial biosynthesis and reduced the effects of baicalein on reversing TAM resistance. Our results indicate that baicalein is a promising candidate to help overcome TAM resistance by sensitizing resistant cells to TAM‐induced growth inhibition and apoptosis. The mechanism underlying the effects of baicalein consists of inhibition of HIF‐1α–mediated aerobic glycolysis and mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
28. Plasma extracellular vesicle‑packaged microRNAs as candidate diagnostic biomarkers for early‑stage breast cancer
- Author
-
Chen Yan, Min Ma, Nan Xu, Yipeng Yang, Hong Hu, Dongxian Zhou, and Jintao Hu
- Subjects
0301 basic medicine ,Cancer Research ,Breast Neoplasms ,Kaplan-Meier Estimate ,Biology ,Biochemistry ,Extracellular Vesicles ,03 medical and health sciences ,breast cancer ,0302 clinical medicine ,Breast cancer ,microRNA ,Biomarkers, Tumor ,Genetics ,medicine ,Extracellular ,Humans ,Circulating MicroRNA ,Molecular Biology ,Early Detection of Cancer ,plasma ,Neoplasm Staging ,Oncogene ,Gene Expression Profiling ,Area under the curve ,Cancer ,tissue ,Articles ,Extracellular vesicle ,Prognosis ,medicine.disease ,Gene expression profiling ,MicroRNAs ,030104 developmental biology ,ROC Curve ,Oncology ,Case-Control Studies ,030220 oncology & carcinogenesis ,Cancer research ,biomarker ,Molecular Medicine ,Female ,extracellular vesicle - Abstract
Extracellular vesicle-packaged microRNAs (miRNAs) are a class of circulating miRNAs located in the plasma that are packaged into extracellular vesicles. The present study examined the expression profiles of extracellular vesicles and tissue miRNAs with the aim of investigating the miRNA signatures in early-stage breast cancer. The present study identified and compared the extracellular vesicle-packaged miRNA expression signature and tissue miRNA expression signature from healthy individuals (n=10) and patients with early-stage breast cancer (n=12). A total of five miRNAs, including miRNA-375, miRNA-24-2-5p, miRNA-548b-5p, miRNA-655-3P and miRNA-376b-5p, were synchronized in extracellular vesicles and tissues of the breast cancer group when compared with the healthy group. The highest area under the curve (AUC) for a single miRNA was achieved with miRNA-548b-5p [AUC=0.785; 95% confidence interval (CI)=0.585–0.984; P=0.022]. The highest overall AUC was achieved by the combination of miRNA-375, miRNA-655-3p, miRNA-548b-5p and miRNA-24-2-5p (AUC=0.808; 95% CI=0.629–0.986; P=0.013). The Kaplan-Meier curves and log test analysis results of these five miRNAs, especially those for miRNA-548b-5p, were partly consistent with the hypothesis. Two miRNAs (miRNA-548b-5p and miRNA-376b-5p) were positively associated with patient survival, while two miRNAs (miRNA-375 and miRNA-24-2-5p) were negatively associated with patient survival. The present study provided a set of plasma extracellular vesicle-packaged miRNA-based biomarkers for the diagnosis of early-stage breast cancer.
- Published
- 2019
29. Recent treatment progress of triple negative breast cancer
- Author
-
Lu Hui-Meng, Gong Zi-Qian, Yang Chang-Qing, Zhao Shi-Qi, Zhang Chen-Yan, Zhao Gang, Liu Jie, Yin Dachuan, Zhou Ren-Bin, Xu Ran, and Zhu Kun
- Subjects
Oncology ,medicine.medical_specialty ,Chemotherapy ,Side effect ,business.industry ,medicine.medical_treatment ,Biophysics ,Estrogen receptor ,Triple Negative Breast Neoplasms ,Disease ,medicine.disease ,Prognosis ,Metastasis ,Breast cancer ,Internal medicine ,Progesterone receptor ,medicine ,Humans ,Neoplasm Metastasis ,business ,Molecular Biology ,Triple-negative breast cancer ,Signal Transduction - Abstract
Breast cancer (BC) is a serious worldwide disease that threatens women's health. Particularly, the morbidity of triple-negative breast cancer (TNBC) is higher than that of other BC types due to its high molecular heterogeneity, metastatic potential and poor prognosis. TNBC lacks of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), so there are still no effective treatment methods for TNBC. Here, we reviewed the classification of TNBC, its molecular mechanisms of pathogenesis, treatment methods and prognosis. Finding effective targets is critical for the treatment of TNBC. Also, refining the classification of TNBC is benefited to choose the treatment of TNBC, because the sensitivity of chemotherapy is different in different TNBC. Some new treatment methods have been proposed in recent years, such as nutritional therapy and noncoding RNA treatment methods. There are some disadvantages, such as the side effect on normal cells after nutrient deprivation, low specificity and instability of noncoding RNA. More studies are necessary to improve the treatment of TNBC.
- Published
- 2019
30. Comparison of the roles of estrogens and androgens in breast cancer and prostate cancer
- Author
-
Gang Zhao, Wen-Jing Liu, Chen-Yan Zhang, Da-Chuan Yin, Kun Zhu, Hui-Meng Lu, Zhao Shiqi, Chang-Qing Yang, Jin Li, Xiang-Bin Zeng, and Sheng-Xiang Lin
- Subjects
0301 basic medicine ,Male ,Risk ,medicine.drug_class ,Cell ,Breast Neoplasms ,urologic and male genital diseases ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,Breast cancer ,Prostate ,Cell Line, Tumor ,Medicine ,Animals ,Humans ,Phosphorylation ,Molecular Biology ,Dose-Response Relationship, Drug ,Estradiol ,business.industry ,Prostatic Neoplasms ,Estrogens ,Cell Biology ,Androgen ,medicine.disease ,3. Good health ,Androgen receptor ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,medicine.anatomical_structure ,Receptors, Estrogen ,Estrogen ,Receptors, Androgen ,030220 oncology & carcinogenesis ,Cancer research ,Androgens ,Female ,business ,Carcinogenesis ,Signal Transduction - Abstract
Breast cancer (BC) and prostate cancer (PC) are the second most common malignant tumors in women and men in western countries, respectively. The risks of death are 14% for BC and 9% for PC. Abnormal estrogen and androgen levels are related to carcinogenesis of the breast and prostate. Estradiol stimulates cancer development in BC. The effect of estrogen on PC is concentration-dependent, and estrogen can regulate androgen production, further affecting PC. Estrogen can also increase the risk of androgen-induced PC. Androgen has dual effects on BC via different metabolic pathways, and the role of the androgen receptor (AR) in BC also depends on cell subtype and downstream target genes. Androgen and AR can stimulate both primary PC and castration-resistant PC. Understanding the mechanisms of the effects of estrogen and androgen on BC and PC may help us to improve curative BC and PC treatment strategies.
- Published
- 2019
31. Exploration of the Potential Mechanism of Tao Hong Si Wu Decoction for the Treatment of Breast Cancer Based on Network Pharmacology and In Vitro Experimental Verification.
- Author
-
Huang, Shi, Chen, Yan, Pan, Lingyu, Fei, Changyi, Wang, Ni, Chu, Furui, Peng, Daiyin, Duan, Xianchun, and Wang, Yongzhong
- Subjects
BREAST cancer ,INHIBITION of cellular proliferation ,BRCA genes ,CANCER treatment ,CHINESE medicine - Abstract
Background: Tao Hong Si Wu Decoction (THSWD) is a well-known traditional Chinese medicine used clinically alone or combined with drugs to treat breast cancer. However, there has been no study to date on the underlying mechanisms of its therapeutic effects. Objectives: To explore the potential mechanism of THSWD for the treatment of breast cancer using network pharmacology and experimental research. Methods: The active ingredients of THSWD were screened according to Lipinski's rule of five based on the 107 ingredients of THSWD identified by UPLC-Q-TOF-MS
E . The targets of THSWD and breast cancer from multiple databases were collected, and a Compound-Target-Pathway network based on protein-protein interaction (PPI) was constructed. Gene ontology (GO) analysis and KEGG pathway analysis were performed via the DAVID server. Molecular docking studies verified the selected key ingredients and key targets. The results of network pharmacology were verified by in vitro experiments. Including the effects of THSWD drug-containing rat serum (THSWD serum) on cell proliferation, and on the targets HRAS, MAPK1, AKT1, GRB2, and MAPK14 were assayed by RT-qPCR and Western blot assays. Results: In total, 27 active ingredients including 8 core components, were obtained from 107 ingredients and 218 THSWD target genes for the treatment of breast cancer were identified. THSWD is active in the treatment of breast cancer by targeting Ras, FoxO, PI3K-Akt and other signaling pathways. MCF-7 and MDA-MB-231 cell proliferation was inhibited by THSWD serum in a time and concentration dependent manner. THSWD could regulated the RNA and protein expression of core targets HRAS, MAPK1, AKT1, GRB2, and MAPK14 for treatment of breast cancer. Conclusion: The results of network pharmacology study showed that THSWD is active against breast cancer by intervening with multiple targets and pathways. Luteolin, kaempferol, senkyunolide E, and other 8 compounds may be the core active ingredients of THSWD in the treatment of breast cancer. THSWD treatment of breast cancer may be related to targeting Ras, FoxO, PI3K-Akt, and other signal pathways associated with the core targets HRAS, MAPK1, AKT1, GRB2, and MAPK14. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
32. Classification of PR-positive and PR-negative subtypes in ER-positive and HER2-negative breast cancers based on pathway scores.
- Author
-
Hu, Taobo, Chen, Yan, Liu, Yiqiang, Zhang, Danhua, Pan, Jiankang, and Long, Mengping
- Subjects
- *
BREAST cancer , *GROWTH factors , *IMMUNOREGULATION , *CELL metabolism , *PROGNOSIS - Abstract
Purpose: PR loss in ER+/HER2- breast cancer indicates worse prognosis and insensitivity to anti-estrogen therapy, while the mechanisms of PR loss in ER+/HER2- breast cancer remain unrevealed.Methods: In this study, ER+/PR+/HER2- and ER+/PR-/HER2- breast cancer cases from TCGA were used. 1387 pathways were analyzed and used as variables for classifying the two groups with LASSO regression.Results: ER+/PR+/HER2- and ER+/PR-/HER2- breast cancer groups can be classified by a combination of 13 pathways using their activity score. Among the 13 pathways, those involving growth factors and ion-channel transporters were most significant in the distinction, followed by pathways involving immune modulation and cell metabolism. Two growth factor pathways, EGF and IGF-1, were deferentially regulated in ER+/PR+/HER2- and ER+/PR-/HER2- groups.Conclusions: In conclusion, this study indicated in ER+/HER2- breast cancers the various status of PR expression can be an indication of molecular variation, particularly for the growth factor pathway activation. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
33. Comprehensive analysis of immune evasion in breast cancer by single-cell RNA-seq
- Author
-
Jianhua Yin, Zhisheng Li, Chen Yan, Enhao Fang, Ting Wang, Hanlin Zhou, Weiwei Luo, Qing Zhou, Jingyu Zhang, Jintao Hu, Haoxuan Jin, Lei Wang, Xing Zhao, Jiguang Li, Xiaojuan Qi, Wenbin Zhou, Chen Huang, Chenyang He, Huanming Yang, Karsten Kristiansen, Yong Hou, Shida Zhu, Dongxian Zhou, Ling Wang, Michael Dean, Kui Wu, Hong Hu, and Guibo Li
- Subjects
Transcriptome ,Cell type ,Tumor microenvironment ,Stromal cell ,medicine.anatomical_structure ,Immune system ,Breast cancer ,Cancer cell ,Cell ,medicine ,Cancer research ,Biology ,medicine.disease - Abstract
The tumor microenvironment is composed of numerous cell types, including tumor, immune and stromal cells. Cancer cells interact with the tumor microenvironment to suppress anticancer immunity. In this study, we molecularly dissected the tumor microenvironment of breast cancer by single-cell RNA-seq. We profiled the breast cancer tumor microenvironment by analyzing the single-cell transcriptomes of 52,163 cells from the tumor tissues of 15 breast cancer patients. The tumor cells and immune cells from individual patients were analyzed simultaneously at the single-cell level. This study explores the diversity of the cell types in the tumor microenvironment and provides information on the mechanisms of escape from clearance by immune cells in breast cancer.One Sentence SummaryLandscape of tumor cells and immune cells in breast cancer by single cell RNA-seq
- Published
- 2018
34. Natural product toosendanin reverses the resistance of human breast cancer cells to adriamycin as a novel PI3K inhibitor
- Author
-
Yin Fang-Zhou, Shan Yating, Hua Bao-jin, Ma Lin, Chen Yan, Wang Kai, Yang Kaiyong, and Yin Wu
- Subjects
0301 basic medicine ,Drug ,media_common.quotation_subject ,Antineoplastic Agents ,Apoptosis ,Breast Neoplasms ,P110α ,Immunofluorescence ,Biochemistry ,Cell Line ,03 medical and health sciences ,Phosphatidylinositol 3-Kinases ,0302 clinical medicine ,Breast cancer ,Downregulation and upregulation ,medicine ,Animals ,Humans ,skin and connective tissue diseases ,PI3K/AKT/mTOR pathway ,media_common ,Pharmacology ,Mice, Inbred BALB C ,medicine.diagnostic_test ,Molecular Structure ,Chemistry ,Neoplasms, Experimental ,medicine.disease ,Multiple drug resistance ,030104 developmental biology ,Doxorubicin ,Drug Resistance, Neoplasm ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Female ,Drugs, Chinese Herbal ,Phytotherapy - Abstract
Adriamycin (ADM) is a commonly used drug in clinical breast cancer treatment. However, some breast cancer types or breast cancers subjected to repeated ADM exposure develop strong resistance to ADM thus limiting its clinical efficacy. In this study, we found for the first time that toosendanin (TSN), a triterpenoid extracted from the traditional Chinese medicine Melia toosendan Sieb et Zucc, could successfully reverse adriamycin resistance in human breast cancer cells. Immunofluorescence and HPLC analysis demonstrated that TSN promoted adriamycin accumulation in breast cancer cells, especially in the nucleus. Furthermore, TSN could significantly reduce ABCB1 expression. We then found that TSN was capable of suppressing adriamycin-induced Akt phosphorylation, probably due to downregulation of the PI3K catalytic subunits P110α and P110β, and inhibition of DNA-PKcs. Importantly, the inhibitory effect of TSN on PI3K P110α and P110β expression was specifically observed in breast cancer cells but not in normal human cells. Moreover, TSN significantly potentiated the anti-cancer effect of ADM in the 4T1 breast cancer model and its inhibition rate was nearly 90%. Thus, TSN could be used as a novel PI3K inhibitor to reverse breast cancer resistance. The combination of ADM and TSN may represent a useful strategy for human breast cancer therapy.
- Published
- 2017
35. The Value of Shear Wave Elastography Quantitative Parameters in the Differentiation of Benign and Malignant Breast Masses and the Prediction of Post-operative Recurrence of Breast Cancer.
- Author
-
CHEN Yan, PENG Guoping, MIN Jie, and LIN Jing
- Subjects
SHEAR waves ,CANCER relapse ,BREAST cancer ,CANCER diagnosis ,ELASTOGRAPHY - Abstract
This paper discusses the effect of shear wave elastography quantitative parameters on the diagnosis and prognosis of breast cancer. Sixty cases of breast cancer patients were taken as the observation group, and 60 cases of benign breast nodules were taken as the control group. The maximum elastic modulus (Emax) were collected for ultrasonic examination using shear wave elastography. T test was used to analyze the difference of Emax between the two groups, and ROC curve was used to analyze the value of Emax in the diagnosis of breast cancer. The results showed that compared with the control group, AE max, Shelllemax, shell2emax and Shell3emax in the observation group were increased. AE max, Shelllemax, Shell2emax and Shell3emax had certain value in the diagnosis of breast cancer. The area under the curve was 0.723, 0.893, 0.818 and 0.791, respectively. AE max, Shelllemax, Shell2emax and Shell3emax had certain value in the diagnosis of postoperative recurrence of breast cancer. The area under the curve was 0.754, 0.884, 0.824 and 0.782, respectively. It is concluded that the quantitative analysis of shear wave elastography has certain value in the diagnosis of breast cancer and prediction of prognosis. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
36. Elevated heparanase expression is associated with poor prognosis in breast cancer : a study based on systematic review and TCGA data
- Author
-
Shijian Chen, Yi Zhang, Xu Sun, Lin Yang, Jin-Ping Li, Pei-Yu Cheng, Jiayun Nian, Gan-Lin Zhang, Guo-Wang Yang, Hui Meng, Xiaomin Wang, Mingwei Yu, Chen Yan, and Yunfei Ma
- Subjects
0301 basic medicine ,Oncology ,Gerontology ,medicine.medical_specialty ,Poor prognosis ,Breast Neoplasms ,Lymph node metastasis ,Traditional Chinese medicine ,Review ,Metastasis ,heparanase ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,breast cancer ,Internal medicine ,medicine ,Biomarkers, Tumor ,Odds Ratio ,Humans ,Heparanase ,Glucuronidase ,Neoplasm Staging ,Cancer och onkologi ,Tumor size ,business.industry ,Odds ratio ,medicine.disease ,Prognosis ,humanities ,Gene Expression Regulation, Neoplastic ,Patient Outcome Assessment ,030104 developmental biology ,030220 oncology & carcinogenesis ,Cancer and Oncology ,Female ,prognosis ,Neoplasm Grading ,business ,Publication Bias - Abstract
// Xu Sun 1 , Ganlin Zhang 1 , Jiayun Nian 1,2 , Mingwei Yu 1 , Shijian Chen 3 , Yi Zhang 1 , Guowang Yang 1 , Lin Yang 1 , Peiyu Cheng 1 , Chen Yan 1,2 , Yunfei Ma 1 , Hui Meng 1,2 , Xiaomin Wang 1 and Jin-Ping Li 1,4 1 Department of Oncology, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing, China 2 School of Graduates, Beijing University of Chinese Medicine, Beijing, China 3 Department of Neurology, Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, China 4 Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden Correspondence to: Xiaomin Wang, email: // Keywords : heparanase, breast cancer, prognosis Received : September 09, 2016 Accepted : March 10, 2017 Published : March 25, 2017 Abstract Heparanase promotes tumorigenesis, angiogenesis, and metastasis. Here, we conducted a study based on systematic review and the Cancer Genome Atlas (TCGA) data that examined heparanase expression in clinical samples to determine its prognostic value. According to the meta-analysis and TCGA data, we found that heparanase expression was up-regulated in most breast cancer specimens, and elevated heparanase expression was associated with increased lymph node metastasis, larger tumor size, higher histological grade, and poor survival. These results suggest that targeting heparanase might improve treatments for breast cancer patients.
- Published
- 2017
37. Abstract 140: Comprehensive analysis of immune evasion in breast cancer by single-cell RNA-seq
- Author
-
Chen Huang, Hanlin Zhou, Ling Wang, Yong Hou, Ruqian lv, Jianhua Yin, Hong Hu, Shida Zhu, Guibo Li, Chenyang He, Michael Dean, Ting Wang, Kui Wu, and Chen Yan
- Subjects
Cancer Research ,Tumor microenvironment ,Stromal cell ,medicine.medical_treatment ,Cell ,Cancer ,Immunotherapy ,Biology ,medicine.disease ,Immune system ,Breast cancer ,medicine.anatomical_structure ,Oncology ,Cancer cell ,Cancer research ,medicine - Abstract
The tumor microenvironment is composed of numerous cell types, including tumor, immune and stromal cells. Cancer cells interact with the tumor microenvironment to suppress anticancer immunity. In this study, we molecularly dissected the tumor microenvironment of breast cancer by single-cell RNA-seq. The breast tumor microenvironment was profiled by analyzing the single-cell transcriptomes of 52,163 cells from the tumor tissues of 15 breast cancer patients. The tumor cells and immune cells from individual patients were analyzed simultaneously at the single-cell level. Among more than 40,000 tumor cells, we identified distinct cell clusters with different molecular subtypes and gene signatures in the same tumor, which revealed intra-tumor heterogeneity in breast cancer. We comprehensively profiled the functional state of T cells, macrophages, B cells, CAFs in breast cancer tumor microenvironment, which highlight the immune cell and CAF diversity in the breast cancer TME. Moreover, we analyzed intercellular communication in the breast cancer TME using a dataset of human ligand receptor pairs, which showed distinct cell interaction models across tumors. The evolution of the tumor microenvironment during clinical treatment was dissected by comparing tumor microenvironment of breast cancer pre- and post-chemotherapy. This study investigated the diversity of the cell types in the tumor microenvironment and provided information on the mechanisms of escape from clearance by immune cells in breast cancer, which could be a beneficial resource for immunotherapy development. Citation Format: Jianhua Yin, Hanlin Zhou, Chen Yan, Ruqian lv, Ting Wang, Chenyang He, Chen Huang, Yong Hou, Shida Zhu, Ling Wang, Michael Dean, Kui Wu, Hong Hu, Guibo Li. Comprehensive analysis of immune evasion in breast cancer by single-cell RNA-seq [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 140.
- Published
- 2019
38. Prognostic value of the systemic inflammation response index (SIRI) before and after surgery in operable breast cancer patients.
- Author
-
Wang, Lei, Zhou, Yehui, Xia, Suhua, Lu, Linlin, Dai, Tiantian, Li, Aoshuang, Chen, Yan, and Gao, Erli
- Subjects
BREAST cancer surgery ,CANCER patients ,LYMPHOCYTE count ,BREAST cancer prognosis ,BREAST cancer ,ABSOLUTE value - Abstract
BACKGROUND: The new systemic inflammation response index (SIRI) constructed based on neutrophil, monocyte and lymphocyte counts in peripheral blood is considered to be related to the prognosis of a variety of tumours. OBJECTIVE: To evaluate the prognostic value of the SIRI in operable breast cancer patients and establish a nomogram to predict the survival of breast cancer patients. METHODS: A total of 949 patients with operable breast cancer were enrolled in the present study. RESULTS: The overall survival (OS) of breast cancer patients with SIRI ⩽ 0.65 was significantly higher than that of breast cancer patients with SIRI > 0.65 (P < 0.001). A nomogram generated based on SIRI, grade and TNM stage and SIRI predicted the 5- and 10-year survival rates of breast cancer patients more accurately than TNM stage alone. In addition, the change in SIRI relative to baseline at 4 weeks after surgery was closely related to the survival of breast cancer patients. Compared with those with no SIRI changes (absolute value of variation < 25%), breast cancer patients with an increase in SIRI > 75% or 25–75% had worse OS (P < 0.001). CONCLUSIONS: The SIRI before and after surgery is closely related to the prognosis of breast cancer patients. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
39. MicroRNA‐425‐5p promotes breast cancer cell growth by inducing PI3K/AKT signaling.
- Author
-
Zhang, Li‐Feng, Zhang, Ji‐Gang, Zhou, Hao, Dai, Tian‐Tian, Guo, Feng‐Bao, Xu, Shao‐Yong, and Chen, Yan
- Subjects
CANCER cell growth ,BREAST cancer ,BREAST cancer prognosis ,MICRORNA ,PTEN protein ,PHOSPHATIDYLINOSITOL 3-kinases ,PROTEIN kinase B - Abstract
MicroRNA‐425‐5p (miR‐425‐5p) has been reported to be involved in the tumorigenesis of several tumors, but its function in breast cancer is still unknown. In this study, miR‐425‐5p was found significantly upregulated in breast cancer cells, and predicted a poor prognosis for breast cancer patients. Overexpression of miR‐425‐5p could significantly promote breast cancer cell growth. Further studies showed that overexpression of miR‐425‐5p upregulated the protein levels of Cyclin D1, Cyclin D3, CDK4, and CDK6. However, inhibiting miR‐425‐5p downregulated their expression and induced cell cycle arrest at G0/G1 phase. In mechanism, overexpression of miR‐425‐5p increased the phosphorylation of PI3K p85 and AKT, but inhibiting miR‐425‐5p displayed opposite effects. Moreover, miR‐425‐5p bound to the 3'UTR of PTEN mRNA, and downregulated the expression levels of PTEN in both mRNA and protein levels in breast cancer cells. Collectively, the results above demonstrated that miR‐425‐5p was involved in the tumorigenesis of breast cancer by inducing PI3K/AKT signaling and indicated that miR‐425‐5p could be as a potential target for breast cancer therapy in the future. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
40. The efficacy and safety of targeted therapy plus fulvestrant in postmenopausal women with hormone-receptor positive advanced breast cancer: A meta-analysis of randomized-control trials
- Author
-
Shi Fang-fang, Chen Yan, Gu Xiaoyi, Gao Chanchan, and Su Xiangyu
- Subjects
Oncology ,Receptor, ErbB-2 ,medicine.medical_treatment ,Cancer Treatment ,lcsh:Medicine ,Toxicology ,Pathology and Laboratory Medicine ,Biochemistry ,Targeted therapy ,law.invention ,Database and Informatics Methods ,Mathematical and Statistical Techniques ,0302 clinical medicine ,Randomized controlled trial ,law ,Breast Tumors ,Medicine and Health Sciences ,Molecular Targeted Therapy ,030212 general & internal medicine ,Database Searching ,lcsh:Science ,Fulvestrant ,Randomized Controlled Trials as Topic ,Multidisciplinary ,Endocrine Therapy ,Combined Modality Therapy ,Postmenopause ,Treatment Outcome ,Receptors, Estrogen ,Research Design ,030220 oncology & carcinogenesis ,Physical Sciences ,Female ,Statistics (Mathematics) ,Research Article ,medicine.drug ,medicine.medical_specialty ,Antineoplastic Agents, Hormonal ,Combination therapy ,Clinical Research Design ,Breast Neoplasms ,Research and Analysis Methods ,03 medical and health sciences ,Breast cancer ,Internal medicine ,Breast Cancer ,medicine ,Humans ,Statistical Methods ,Adverse effect ,Toxicity ,business.industry ,lcsh:R ,Cancers and Neoplasms ,Biology and Life Sciences ,Cancer ,Publication bias ,medicine.disease ,Survival Analysis ,Hormones ,lcsh:Q ,Adverse Events ,business ,Mathematics ,Meta-Analysis - Abstract
Objective To evaluate the efficacy and safety of targeted therapy plus fulvestrant for postmenopausal patients with hormone receptor-positive advanced breast cancer. Methods Pubmed, Embase and Web of Science databases were systematically searched on February 26, 2018. Eligible studies were screened according to selection criteria, and two reviewers independently extracted outcome data which included progression-free survival, overall survival, objective response rate, clinical benefit rate and toxicities. RevMan 5.3 and STATA 11.0 software were used to conduct meta-analysis. Results Thirteen articles including twelve randomized-control trials fulfilled selection criteria. There was no evidence regarding the existence of publication bias and high-risk bias of quality in the selected studies. In previously endocrine therapy-treated postmenopausal patients with hormone-receptor positive advanced breast cancer, the PFS (HR = 0.77, 95%CI: 0.66-0.91) and ORR (RR = 1.78, 95%CI: 1.35-2.34) of combination therapy group were significantly higher than that from fulvestrant monotherapy group. Besides, a statistically significant difference in PFS was found across the two arms in postmenopausal women with PIK3CA-mutant ctDNA tumor (HR = 0.52, 95% CI: 0.39-0.69). Moreover, the risk of adverse events (RR = 1.09, 95%CI: 1.05-1.13), CTCAE≥3 (RR = 1.97, 95%CI: 1.49-2.60) and discontinuation due to adverse events (RR = 4.91, 95%CI: 3.37-7.15) were also significantly different between two treatment groups. Sensitivity analysis showed PLOMA-3 trial was an important factor of heterogeneity. Discussion Even though the combination of targeted therapy plus fulvestrant improved PFS and increased ORR in advanced breast cancer patients, the toxicities of combination therapy were also higher than fulvestrant monotherapy. Further studies related to inhibitors targeting the specific signaling pathway or receptors are urgently needed, and more efforts concerning precision medicine of targeted therapy plus endocrine therapy should be taken to improve the clinical benefits.
- Published
- 2018
41. A new targeting approach for breast cancer gene therapy using the human fatty acid synthase promoter
- Author
-
Zhang Rui, Han Hua, Liu Wen-chao, Qin Hong-Yan, Jin Wei-Lin, and Chen Yan
- Subjects
Recombinant Fusion Proteins ,Genetic enhancement ,Genetic Vectors ,Gene Expression ,Antineoplastic Agents ,Breast Neoplasms ,In Vitro Techniques ,Biology ,Breast cancer ,medicine ,Humans ,Cytotoxic T cell ,Radiology, Nuclear Medicine and imaging ,Treatment Failure ,Ganciclovir ,Midkine ,Adenoviruses, Human ,Tumor Suppressor Proteins ,Genes, Transgenic, Suicide ,Nuclear Proteins ,Cancer ,Genetic Therapy ,Hematology ,General Medicine ,Suicide gene ,Prognosis ,medicine.disease ,Molecular biology ,DNA-Binding Proteins ,Phenotype ,Treatment Outcome ,Oncology ,Thymidine kinase ,Cancer cell ,biology.protein ,Cancer research ,Female ,Fatty Acid Synthases - Abstract
Gene therapy with adenoviral vectors is a promising new approach for the treatment of refractory advanced breast cancer. Strategies to restrict adenoviral-mediated therapeutic gene expression are important to avoid harming normal cells. Fatty acid synthase (FAS) is overexpressed in several human cancers. FAS is highly expressed in infiltrating breast cancer tissue, and always associated with malignant phenotypes and poor prognosis. In this study, expression of the FAS was evaluated in three breast cancer cell lines. A 680 bp-FAS promoter was cloned and its transcriptional activity was analyzed in breast cancer cell lines. We made a recombinant adenovirus construct carrying herpes simplex virus thymidine kinase (HSV-TK) driven by human FAS promoter (Ad-FAS-TK) and analyzed its target cytotoxicity in vitro and in vivo against human breast cancer cells combined with prodrug ganciclovir (GCV). The results show that the expression of FAS varies in the three breast cancer cell lines examined (respectively, SK-Br3>MCF-7>MDA-MB-231), but FAS promoter can initiate relative high transcriptional activities in all three kinds of cancer cells while little in normal fibroblast cells. Furthermore, FAS promoter can drive the therapeutic gene in a wider range of human breast cancers than cerbB2 promoter and exhibit a stronger activity than midkine (MK) promoter. Combination of Ad-FAS-TK and GCV treatment exhibited strong-targeted cytotoxic effect on breast cancer cells but showed little activity in normal fibroblast cells. The tumorigenic capability of breast cancer cells treated with Ad-FAS-TK/GCV was completely inhibited in vitro and in vivo assays. In conclusion, adenoviral-mediated suicide gene therapy controlled by tumor associated-FAS promoter can induce specific cytotoxic effect on human breast cancer cells in vitro and in vivo. So it is a promising target for the development of gene therapy against breast cancers.
- Published
- 2007
42. Effects of RNA interference‐mediated silencing of toll‐like receptor 4 gene on proliferation and apoptosis of human breast cancer MCF‐7 and MDA‐MB‐231 cells: An in vitro study.
- Author
-
Gao, Xiao‐Ling, Yang, Jiao‐Jiao, Wang, Shu‐Juan, Chen, Yan, Wang, Bei, Cheng, Er‐Jing, Gong, Jian‐Nan, Dong, Yan‐Ting, Liu, Dai, Wang, Xiang‐Li, Huang, Ya‐Qiong, and An, Dong‐Dong
- Subjects
RNA interference ,BREAST cancer ,CANCER cells ,CANCER chemotherapy ,GENE expression - Abstract
Breast cancer is known as the most prevalent cancer in women worldwide, and has an undeniable negative impact on public health, both physically, and mentally. This study aims to investigate the effects of toll‐like receptor 4 (TLR4) gene silencing on proliferation and apoptosis of human breast cancer cells to explore for a new theoretical basis for its treatment. TLR4 small interference RNA (siRNA) fragment recombinant plasmids were constructed, including TLR4 siRNA‐1, TLR4 siRNA‐2, and TLR4 siRNA‐3. Human breast cancer MCF‐7 and MDA‐MB‐231 cells were assigned into blank, negative control (NC), TLR4 siRNA‐1, TLR4 siRNA‐2, and TLR4 siRNA‐3 groups. MCF‐7 and MDA‐MB‐231 cell growth was detected by MTT assay. Apoptosis and cell cycle were determined by flow cytometry. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blot analysis were conducted to determine the expression of TLR4, CDK4, cyclin D1, Livin, Bcl‐2, p53, c‐FLIP, and caspase‐3. In comparison with the NC and blank groups, the TLR4 siRNA‐1, TLR4 siRNA‐2, and TLR4 siRNA‐3 groups showed decreased the expression of TLR4, inhibited proliferation of MCF‐7 and MDA‐MB‐231 cells and promoted MCF‐7 and MDA‐MB‐231 cell apoptosis, and the cells were blocked in G1 phase. In comparison with the NC and blank groups, in the TLR4 siRNA‐1, TLR4 siRNA‐2, and TLR4 siRNA‐3 groups, siRNA‐TLR4 significantly increased expression of p53 and caspase‐3 in MCF‐7 and MDA‐MB‐231 cells, while it decreased the expressions of CDK4, cyclinD1, Livin, Bal‐2, and c‐FLIP. The study demonstrates that TLR4 gene silencing inhibits proliferation and induces apoptosis of MCF‐7 and MDA‐MB‐231 cells. TLR4 gene silencing inhibits proliferation and induces apoptosis of MCF‐7 and MDA‐MB‐231 cells. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
43. Reductive 17beta-hydroxysteroid dehydrogenases which synthesize estradiol and inactivate dihydrotestosterone constitute major and concerted players in ER+ breast cancer cells
- Author
-
Chen-Yan Zhang, Sheng-Xiang Lin, Jiong Chen, and Wei-Qi Wang
- Subjects
medicine.medical_specialty ,17-Hydroxysteroid Dehydrogenases ,medicine.drug_class ,Cell Survival ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Biology ,Biochemistry ,Flow cytometry ,Estradiol Dehydrogenases ,03 medical and health sciences ,0302 clinical medicine ,Endocrinology ,Breast cancer ,Internal medicine ,Cell Line, Tumor ,medicine ,Humans ,MTT assay ,Viability assay ,RNA, Small Interfering ,skin and connective tissue diseases ,Molecular Biology ,030304 developmental biology ,Cell Proliferation ,Feedback, Physiological ,0303 health sciences ,medicine.diagnostic_test ,Estradiol ,Cell growth ,Cell Cycle ,Estrogen Receptor alpha ,Cancer ,Dihydrotestosterone ,Cell Biology ,Cell cycle ,medicine.disease ,Gene Expression Regulation, Neoplastic ,Estrogen ,030220 oncology & carcinogenesis ,Cancer research ,MCF-7 Cells ,Molecular Medicine ,hormones, hormone substitutes, and hormone antagonists ,Signal Transduction - Abstract
The reductive 17β-hydroxysteroid dehydrogenases which catalyze the last step in estrogen activation for estrogen dependent breast cancer cells were studied. Their biological function and the effects of their knockdown for cancer cell proliferation were demonstrated. The multidisciplinary study involves enzyme catalysis, sex-hormone and cell cycle regulation, as well as cell proliferation in breast cancer cells. Reductive 17β-HSD1, -7 and -12 were studied in the main breast cancer epithelial cells MCF-7 and T47D. Modification of estradiol and 5α-dihydrotestosterone concentrations was monitored by ELISA assay while corresponding cell viability measured by MTT assay. Cell cycle was determined by flow cytometry. Dual activity of estradiol activation and 5α-dihydrotestosterone reduction by 17β-HSD1 and -7 was critical for breast cancer cell (T47D and MCF-7) viability. Cell viability was decreased by 35.8% ± 1.6% in T47D cells after simultaneously knocking down 17β-HSD1 and -7. MCF-7 cell viability was decreased by 29.3% ± 4.2% using a combination of siRNAs and inhibitors. By knocking down 17β-HSD7, we have provided the first demonstration of the significant role of this enzyme in the stimulation of breast cancer cell viability as a result of its high activity on androgen reduction with positive feedback on estradiol production. A further decrease in cell viability was not observed with additional knockdown of 17β-HSD12 after 17β-HSD1 and 7. Breast cancer cell cycle progression was impeded to enter the S phase from G 0 –G 1 after knocking down 17β-HSD1 and -7. In summary, this is the first demonstration that the dual activity in estrone activation and 5α-dihydrotestosterone reduction are the functional basis of reductive 17β-HSDs in breast cancer cells. 17β-HSD1 and -7 are principal reductive 17β-HSDs and major players in the viability of estrogen-dependent breast cancer cells. Combined targeting of these enzymes may be potential for molecular therapy of such cancer.
- Published
- 2014
44. The mTOR inhibitor rapamycin synergizes with a fatty acid synthase inhibitor to induce cytotoxicity in ER/HER2-positive breast cancer cells
- Author
-
Han Sheng, Chen Yan, Huang Wei, Yang Jingyue, Xue Yan, Liu Wen-chao, and Zheng Minjuan
- Subjects
Cell signaling ,Receptor, ErbB-2 ,Physiology ,Papillary Carcinomas ,Tumor Physiology ,Cancer Treatment ,lcsh:Medicine ,Invasive Ductal Carcinoma ,Apoptosis ,Signal transduction ,medicine.disease_cause ,Biochemistry ,chemistry.chemical_compound ,Mice ,Benign Breast Tumors ,Endocrinology ,Cell Movement ,Molecular Cell Biology ,Basic Cancer Research ,Breast Tumors ,Tumor Cells, Cultured ,Morphogenesis ,Medicine and Health Sciences ,Membrane Receptor Signaling ,AKT signaling cascade ,lcsh:Science ,skin and connective tissue diseases ,Fluorescent Antibody Technique, Indirect ,Multidisciplinary ,biology ,Cell Death ,Reverse Transcriptase Polymerase Chain Reaction ,Signaling cascades ,Drug Synergism ,Gene Therapy ,Hormone Receptor Signaling ,Fatty Acid Synthase, Type I ,Gene Expression Regulation, Neoplastic ,Fatty acid synthase ,Cell Motility ,Ductal Carcinoma in Situ ,Oncology ,Selective estrogen receptor modulator ,Cell Processes ,Female ,Invasive Lobular Carcinoma ,Research Article ,medicine.medical_specialty ,Cell biology ,Blotting, Western ,Mice, Nude ,Nipple Tumors ,Breast Neoplasms ,Cell Migration ,Real-Time Polymerase Chain Reaction ,Breast cancer ,Internal medicine ,medicine ,Animals ,Humans ,RNA, Messenger ,Molecular Biology Techniques ,Protein kinase B ,neoplasms ,Protein Kinase Inhibitors ,Molecular Biology ,PI3K/AKT/mTOR pathway ,Cell Proliferation ,Sirolimus ,Biology and life sciences ,Endocrine Physiology ,business.industry ,lcsh:R ,Estrogen Receptor alpha ,Cancers and Neoplasms ,medicine.disease ,Xenograft Model Antitumor Assays ,Cerulenin ,Hormones ,chemistry ,biology.protein ,Cancer research ,lcsh:Q ,business ,Carcinogenesis ,Developmental Biology - Abstract
Patients with ER/HER2-positive breast cancer have a poor prognosis and are less responsive to selective estrogen receptor modulators; this is presumably due to the crosstalk between ER and HER2. Fatty acid synthase (FASN) is essential for the survival and maintenance of the malignant phenotype of breast cancer cells. An intimate relationship exists between FASN, ER and HER2. We hypothesized that FASN may be the downstream effector underlying ER/HER2 crosstalk through the PI3K/AKT/mTOR pathway in ER/HER2-positive breast cancer. The present study implicated the PI3K/AKT/mTOR pathway in the regulation of FASN expression in ER/HER2-positive breast cancer cells and demonstrated that rapamycin, an mTOR inhibitor, inhibited FASN expression. Cerulenin, a FASN inhibitor, synergized with rapamycin to induce apoptosis and inhibit cell migration and tumorigenesis in ER/HER2-positive breast cancer cells. Our findings suggest that inhibiting the mTOR-FASN axis is a promising new strategy for treating ER/HER2-positive breast cancer.
- Published
- 2013
45. MICAL1 facilitates breast cancer cell proliferation via ROS‐sensitive ERK/cyclin D pathway.
- Author
-
Deng, Wenjie, Wang, Yueyuan, Zhao, Shuo, Zhang, Yujie, Chen, Yan, Zhao, Xuyang, Liu, Lei, Sun, Shixiu, Zhang, Lin, Ye, Bixing, and Du, Jun
- Subjects
BREAST cancer ,CELL proliferation ,FLAVOPROTEINS ,CYTOSKELETON ,PHOSPHATIDYL inositol ,CANCER cells - Abstract
Abstract: Molecule interacting with CasL 1 (MICAL1) is a multidomain flavoprotein mono‐oxygenase that strongly involves in cytoskeleton dynamics and cell oxidoreduction metabolism. Recently, results from our laboratory have shown that MICAL1 modulates reactive oxygen species (ROS) production, and the latter then activates phosphatidyl inositol 3‐kinase (PI3K)/protein kinase B (Akt) signalling pathway which regulates breast cancer cell invasion. Herein, we performed this study to assess the involvement of MICAL1 in breast cancer cell proliferation and to explore the potential molecular mechanism. We noticed that depletion of MICAL1 markedly reduced cell proliferation in breast cancer cell line MCF‐7 and T47D. This effect of MICAL1 on proliferation was independent of wnt/β‐catenin and NF‐κB pathways. Interestingly, depletion of MICAL1 significantly inhibited ROS production, decreased p‐ERK expression and unfavourable for proliferative phenotype of breast cancer cells. Likewise, MICAL1 overexpression increased p‐ERK level as well as p‐ERK nucleus translocation. Moreover, we investigated the effect of MICAL1 on cell cycle‐related proteins. MICAL1 positively regulated CDK4 and cyclin D expression, but not CDK2, CDK6, cyclin A and cyclin E. In addition, more expression of CDK4 and cyclin D by MICAL1 overexpression was blocked by PI3K/Akt inhibitor LY294002. LY294002 treatment also attenuated the increase in the p‐ERK level in MICAL1‐overexpressed breast cancer cells. Together, our results suggest that MICAL1 exhibits its effect on proliferation via maintaining cyclin D expression through ROS‐sensitive PI3K/Akt/ERK signalling in breast cancer cells. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
46. Effect of telehealth intervention on breast cancer patients' quality of life and psychological outcomes: A meta-analysis.
- Author
-
Yan-Ya Chen, Bing-Sheng Guan, Ze-Kai Li, Xing-Yi Li, Chen, Yan-Ya, Guan, Bing-Sheng, Li, Ze-Kai, and Li, Xing-Yi
- Subjects
TELEMEDICINE ,BREAST cancer patients ,QUALITY of life ,META-analysis ,MEDICAL innovations ,RANDOMIZED controlled trials ,BREAST tumor treatment ,PREVENTION of mental depression ,BREAST tumors ,MENTAL health ,PATIENT education ,SELF-efficacy ,SYSTEMATIC reviews ,ACTIVITIES of daily living ,CANCER & psychology - Abstract
Introduction Telehealth intervention has been proposed as an innovative intervention approach to breast cancer patients, but there are still conflicting results in the literature about its effect. Methods PubMed, EMBASE, CENTRAL and China National Knowledge Infrastructure (CNKI) were searched from inception to 3 October 2016 for randomized controlled trials (RCTs) which assessed the effect of telehealth intervention versus usual care in breast cancer patients. No language restrictions were used. Standardized mean difference (SMD) with corresponding 95% confidence interval (95% CI) was pooled when needed. Subgroup and sensitivity analyses were conducted if necessary and feasible. Results Twenty RCTs with a total of 2190 participants were included into this meta-analysis. Compared with usual care, telehealth intervention was associated with higher quality of life (SMD = 0.60, 95% CI 0.18-1.01, p = 0.005) and self-efficacy (SMD = 0.59, 95% CI 0.19-0.98, p = 0.003), with less depression (SMD = -1.29, 95% CI -2.28 to -0.30, p = 0.01), distress (SMD = -0.25, 95% CI -0.40 to -0.10, p = 0.001) and perceived stress (SMD = -0.30, 95% CI, -0.59 to -0.02, p = 0.04). However, anxiety score did not differ significantly between the two groups (SMD = -0.09, 95% CI -0.22 to 0.04, p = 0.17). Discussion Telehealth intervention is superior to usual care in breast cancer patients for improved quality of life, higher self-efficacy and less depression, distress, and perceived stress. However, these results should be recognized cautiously due to between-study heterogeneity, indicating that further well-designed RCTs are warranted. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
47. Novel multi-kinase inhibitor, T03 inhibits Taxol-resistant breast cancer.
- Author
-
Li, Yan, Liu, Chunxia, Tang, Ke, Chen, Yan, Tian, Kang, Feng, Zhiqiang, and Chen, Jindong
- Subjects
BREAST cancer ,KINASES ,CANCER cells ,CELL proliferation ,RAPAMYCIN - Abstract
Activation of kinase-associated signaling pathways is one of the leading causes of various malignant phenotypes in breast tumors. Strategies of drug discovery and development have investigated approaches to target the inhibition of protein kinase signaling. In the current study, the anti-tumor activities of a novel multi-kinase inhibitor, T03 were evaluated in breast cancer. T03 inhibited Taxol-resistant breast cancer cell proliferation and induced cell cycle arrest and apoptosis in vitro and in vivo. The current results demonstrated that T03 downregulated c-Raf, platelet-derived growth factor receptor-ß and other kinases, thus inhibited Raf/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase and Akt/mechanistic target of rapamycin survival pathways in MCF-7 and MCF-7/Taxol xenograft tumors. At a dose of 100 mg/kg, T03 inhibited tumor growth by 62.90 and 59.98% in tumor weight in MX-1 and MX-1/T xenograft models, respectively and by 62.60 and 60.22% in MCF-7 and MCF-7/T tumors, respectively. These data indicate that the novel multi-kinase inhibitor, T03, may present as a potential compound to develop novel treatments against breast cancer and Taxol-resistant breast tumors. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
48. Does Breast Reconstruction Impact the Decision of Patients to Pursue Cosmetic Surgery?
- Author
-
Ari M. Wes, Joseph M. Serletti, Stephen J. Kovach, Jesse C. Selber, Liza C. Wu, Chen Yan, Vivian M. Hsu, Jonas A. Nelson, and Youssef Tahiri
- Subjects
medicine.medical_specialty ,Mammaplasty ,medicine.medical_treatment ,Cosmetic Techniques ,Breast cancer ,Patient satisfaction ,Surveys and Questionnaires ,Outcome Assessment, Health Care ,Body Image ,medicine ,Humans ,Mastectomy ,Retrospective Studies ,Motivation ,business.industry ,Retrospective cohort study ,Pennsylvania ,medicine.disease ,Self Concept ,Surgery ,Patient Satisfaction ,Multivariate Analysis ,Female ,Breast reconstruction ,business - Abstract
Breast reconstruction is an integral component of breast cancer treatment, often aiding in restoring a patient's sense of femininity. However, many patients choose to have subsequent cosmetic surgery. The purpose of this study is to investigate the reasons that motivate patients to have cosmetic surgery after breast reconstruction.The authors performed a retrospective study examining patients who had breast reconstruction and subsequent cosmetic surgery at the University of Pennsylvania Health System between January 2005 and June 2012. This cohort received a questionnaire assessing the influences and impact of their reconstructive and cosmetic procedures.A total of 1,214 patients had breast reconstruction, with 113 patients (9.3%) undergoing cosmetic surgery after reconstruction. Of 42 survey respondents, 35 had autologous breast reconstruction (83.3%). Fifty-two cosmetic procedures were performed in survey respondents, including liposuction (26.9%) and facelift (15.4%). The most common reason for pursuing cosmetic surgery was the desire to improve self-image (n = 26, 61.9%), with 29 (69.0%) patients feeling more self-conscious of appearance after reconstruction. Body image satisfaction was significantly higher after cosmetic surgery (P = 0.0081). Interestingly, a multivariate analysis revealed that patients who experienced an improvement in body image after breast reconstruction were more likely to experience a further improvement after a cosmetic procedure (P = 0.031, OR = 17.83). Patients who were interested in cosmetic surgery prior to reconstruction were also more likely to experience an improvement in body image after cosmetic surgery (P = 0.012, OR = 22.63).Cosmetic surgery may improve body image satisfaction of breast reconstruction patients and help to further meet their expectations.
- Published
- 2013
49. Lack of correlation between serum levels of E- and P-cadherin fragments and the presence of breast cancer
- Author
-
Chen Yan Lin, Karen A. Knudsen, Keith R. Johnson, Margaret J. Wheelock, Albert A. Keshgegian, and Alejandro Peralta Soler
- Subjects
medicine.medical_specialty ,Cell adhesion molecule ,Cadherin ,Mammary gland ,Cancer ,Breast Neoplasms ,Enzyme-Linked Immunosorbent Assay ,Biology ,medicine.disease ,Cadherins ,Immunohistochemistry ,Pathology and Forensic Medicine ,Breast cancer ,medicine.anatomical_structure ,Endocrinology ,Internal medicine ,Cancer research ,medicine ,Carcinoma ,Extracellular ,Humans ,Female ,Breast - Abstract
Breast cancers often show reduced expression of the transmembrane cell-cell adhesion protein, E-cadherin. In addition, approximately half of breast carcinomas express P-cadherin, which correlates with poor survival. A large fragment of the E-cadherin extracellular domain can be detected in serum, and it has been proposed that an increase in serum E-cadherin can denote the presence of a tumor. In this study, we tested the possibility that serum E- or P-cadherin levels might be useful diagnostic or prognostic indicators in breast cancer. However, we found no indication that the level of serum E-cadherin correlated with the presence of breast cancer. In addition, although we successfully detected a fragment of P-cadherin in serum, we found that its level was considerably lower than that of E-cadherin and did not correlate with the presence of P-cadherin-positive breast cancer.
- Published
- 2000
50. MICAL1 controls cell invasive phenotype via regulating oxidative stress in breast cancer cells.
- Author
-
Wenjie Deng, Yueyuan Wang, Luo Gu, Biao Duan, Jie Cui, Yujie Zhang, Yan Chen, Shixiu Sun, Jing Dong, Jun Du, Deng, Wenjie, Wang, Yueyuan, Gu, Luo, Duan, Biao, Cui, Jie, Zhang, Yujie, Chen, Yan, Sun, Shixiu, Dong, Jing, and Du, Jun
- Subjects
BREAST cancer patients ,ARYL hydrocarbon hydroxylases ,OXIDATIVE stress ,HELA cells ,CELL migration ,CHEMILUMINESCENCE ,IMMUNOFLUORESCENCE ,IMMUNOBLOTTING ,PROTEIN metabolism ,REACTIVE oxygen species ,BREAST tumors ,CANCER invasiveness ,CARRIER proteins ,CELL lines ,CELL physiology ,CELLS ,CELL motility ,CYTOSKELETAL proteins ,PHOSPHORYLATION ,PROTEINS ,TRANSFERASES - Abstract
Background: Molecules Interacting with CasL (MICAL1), a multidomain flavoprotein monoxygenase, is strongly involved in the mechanisms that promote cancer cell proliferation and survival. Activation of MICAL1 causes an up-regulation of reactive oxygen species (ROS) in HeLa cells. ROS can function as a signaling molecule that modulates protein phosphorylation, leading to malignant phenotypes of cancer cells such as invasion and metastasis. Herein, we tested whether MICAL1 could control cell migration and invasion through regulating ROS in breast cancer cell lines.Methods: The effects of depletion/overexperssion of MICAL1 on cell invasion rate were measured by matrigel-based transwell assays. The contents of ROS in breast cancer cells were evaluated by CM2-DCFHDA staining and enhanced lucigenin chemiluminescence method. RAB35 activity was assessed by pulldown assay. The relationship of RAB35 and MICAL1 was evaluated by immunofluorescence, coimmunoprecipitation, immunoblotting and co-transfection techniques. Immunoblotting assays were also used to analyze Akt phosphorylation level.Results: In this study, we found that depletion of MICAL1 reduced cell migration and invasion as well as ROS generation. Phosphorylation of Akt was also attenuated by MICAL1 depletion. Likewise, the over-expression of MICAL1 augmented the generation of ROS, increased Akt phosphorylation, and favored invasive phenotype of breast cancer cells. Moreover, we investigated the effect of EGF signaling on MICAL1 function. We demonstrated that EGF increased RAB35 activation and activated form of RAB35 could bind to MICAL1. Silencing of RAB35 repressed ROS generation, prevented Akt phosphorylation and inhibited cell invasion in response to EGF.Conclusions: Taken together, our results provide evidence that MICAL1 plays an essential role in the activation of ROS/Akt signaling and cell invasive phenotype and identify a novel link between RAB35 and MICAL1 in regulating breast cancer cell invasion. These findings may provide a basis for designing future therapeutic strategy for blocking breast cancer metastasis. [ABSTRACT FROM AUTHOR]- Published
- 2016
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.