20 results on '"Chunfang Tian"'
Search Results
2. Effects of the gut microbiota and its metabolite short-chain fatty acids on endometriosis
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Menghe Liu, Ru Peng, Chunfang Tian, Jianping Shi, Jiannan Ma, Ruiwen Shi, Xiao Qi, Rongwei Zhao, and Haibin Guan
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gut microbiota ,short-chain fatty acids ,endometriosis ,mechanism of action ,treatment strategy ,Microbiology ,QR1-502 - Abstract
In recent years, a growing body of research has confirmed that the gut microbiota plays a major role in the maintenance of human health and disease. A gut microbiota imbalance can lead to the development of many diseases, such as pregnancy complications, adverse pregnancy outcomes, polycystic ovary syndrome, endometriosis, and cancer. Short-chain fatty acids are metabolites of specific intestinal bacteria and are crucial for maintaining intestinal homeostasis and regulating metabolism and immunity. Endometriosis is the result of cell proliferation, escape from immune surveillance, and invasive metastasis. There is a strong correlation between the anti-proliferative and anti-inflammatory effects of short-chain fatty acids produced by gut microbes and the development of endometriosis. Given that the mechanism of action of gut microbiota and Short-chain fatty acids in endometriosis remain unclear, this paper aims to provide a comprehensive review of the complex interactions between intestinal flora, short-chain fatty acids and endometriosis. In addition, we explored potential microbial-based treatment strategies for endometriosis, providing new insights into the future development of diagnostic tests and prevention and treatment methods for endometriosis.
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- 2024
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3. An evaluation of Astragali Radix with different growth patterns and years, based on a new multidimensional comparison method
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Yapeng Wang, Changsheng Yuan, Jiachen Zhao, Yunxiang Liu, Chunfang Tian, Jinxiu Qian, Tiegui Nan, Liping Kang, Yanmeng Liu, Zhilai Zhan, and Luqi Huang
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Astragali Radix ,growth patterns ,growth years ,quality difference ,imitated-wild cultivation ,Plant culture ,SB1-1110 - Abstract
IntroductionWith the depletion of wild Astragali Radix (WA) resources, imitated-wild Astragali Radix (IWA) and cultivated Astragali Radix (CA) have become the main products of Astragali Radix. However, the quality differences of three growth patterns (WA, IWA, CA) and different growth years of Astragali Radix have not been fully characterized, leading to a lack of necessary scientific evidence for their use as substitutes for WA.MethodsWe innovatively proposed a multidimensional evaluation method that encompassed traits, microstructure, cell wall components, saccharides, and pharmacodynamic compounds, to comprehensively explain the quality variances among different growth patterns and years of Astragali Radix.Results and discussionOur study showed that the quality of IWA and WA was comparatively similar, including evaluation indicators such as apparent color, sectional structure and odor, thickness of phellem, diameter and number of vessels, morphology of phloem and xylem, and the levels and ratios of cellulose, hemicellulose, lignin, sucrose, starch, water-soluble polysaccharides, total-saponins. However, the content of sucrose, starch and sorbose in CA was significantly higher than WA, and the diameter and number of vessels, total-flavonoids content were lower than WA, indicating significant quality differences between CA and WA. Hence, we suggest that IWA should be used as a substitute for WA instead of CA. As for the planting years of IWA, our results indicated that IWA aged 1-32 years could be divided into three stages according to their quality change: rapid growth period (1-5 years), stable growth period (6-20 years), and elderly growth period (25-32 years). Among these, 6-20 years old IWA exhibited consistent multidimensional comparative results, showcasing elevated levels of key active components such as water-soluble polysaccharides, flavonoids, and saponins. Considering both the quality and cultivation expenses of IWA, we recommend a cultivation duration of 6-8 years for growers. In conclusion, we established a novel multidimensional evaluation method to systematically characterize the quality of Astragali Radix, and provided a new scientific perspective for the artificial cultivation and quality assurance of Astragali Radix.
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- 2024
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4. Melatonin synergizes BRAF-targeting agent vemurafenib in melanoma treatment by inhibiting iNOS/hTERT signaling and cancer-stem cell traits
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Jiaojiao Hao, Wenhua Fan, Yizhuo Li, Ranran Tang, Chunfang Tian, Qian Yang, Tianhua Zhu, Chaoliang Diao, Sheng Hu, Manyu Chen, Ping Guo, Qian Long, Changlin Zhang, Ge Qin, Wendan Yu, Miao Chen, Liren Li, Lijun Qin, Jingshu Wang, Xiuping Zhang, Yandong Ren, Penghui Zhou, Lijuan Zou, Kui Jiang, Wei Guo, and Wuguo Deng
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Melatonin ,Vemurafenib ,NF-κB ,iNOS ,hTERT ,Cancer stem cell ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background As the selective inhibitor of BRAF kinase, vemurafenib exhibits effective antitumor activities in patients with V600 BRAF mutant melanomas. However, acquired drug resistance invariably develops after its initial treatment. Methods Immunohistochemical staining was performed to detect the expression of iNOS and hTERT, p-p65, Epcam, CD44, PCNA in mice with melanoma xenografts. The proliferation and migration of melanoma cells were detected by MTT, tumorsphere culture, cell cycle, cell apoptosis, AO/EB assay and colony formation, transwell assay and scratch assay in vitro, and tumor growth differences were observed in xenograft nude mice. Changes in the expression of key molecules in the iNOS/hTERT signaling pathways were detected by western blot. Nucleus-cytoplasm separation, and immunofluorescence analyses were conducted to explore the location of p50/p65 in melanoma cell lines. Flow cytometry assay were performed to determine the expression of CD44. Pull down assay and ChIP assay were performed to detect the binding ability of p65 at iNOS and hTERT promoters. Additionally, hTERT promoter-driven luciferase plasmids were transfected in to melanoma cells with indicated treatment to determine luciferase activity of hTERT. Results Melatonin significantly and synergistically enhanced vemurafenib-mediated inhibitions of proliferation, colony formation, migration and invasion and promoted vemurafenib-induced apoptosis, cell cycle arresting and stemness weakening in melanoma cells. Further mechanism study revealed that melatonin enhanced the antitumor effect of vemurafenib by abrogating nucleus translocation of NF-κB p50/p65 and their binding at iNOS and hTERT promoters, thereby suppressing the expression of iNOS and hTERT. The elevated anti-tumor capacity of vemurafenib upon co-treatment with melatonin was also evaluated and confirmed in mice with melanoma xenografts. Conclusions Collectively, our results demonstrate melatonin synergizes the antitumor effect of vemurafenib in human melanoma by inhibiting cell proliferation and cancer-stem cell traits via targeting NF-κB/iNOS/hTERT signaling pathway, and suggest the potential of melatonin in antagonizing the toxicity of vemurafenib and augmenting its sensitivities in melanoma treatment.
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- 2019
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5. BPTF promotes hepatocellular carcinoma growth by modulating hTERT signaling and cancer stem cell traits
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Xinrui Zhao, Fufu Zheng, Yizhuo Li, Jiaojiao Hao, Zhipeng Tang, Chunfang Tian, Qian Yang, Tianhua Zhu, Chaoliang Diao, Changlin Zhang, Manyu Chen, Sheng Hu, Ping Guo, Lizhi Zhang, Yina Liao, Wendan Yu, Miao Chen, Lijuan Zou, Wei Guo, and Wuguo Deng
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Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Bromodomain PHD finger transcription factor (BPTF), a core subunit of nucleosome-remodeling factor (NURF) complex, plays an important role in chromatin remodeling. However, its precise function and molecular mechanism involved in hepatocellular carcinoma (HCC) growth are still poorly defined. Here, we demonstrated the tumor-promoting role of BPTF in HCC progression. BPTF was highly expressed in HCC cells and tumor tissues of HCC patients compared with normal liver cells and tissues. Knockdown of BPTF inhibited cell proliferation, colony formation and stem cell-like traits in HCC cells. In addition, BPTF knockdown effectively sensitized the anti-tumor effect of chemotherapeutic drugs and induced more apoptosis in HCC cells. Consistently, knockdown of BPTF in a xenograft mouse model also suppressed tumor growth and metastasis accompanied by the suppression of cancer stem cells (CSC)-related protein markers. Moreover, the mechanism study showed that the tumor-promoting role of BPTF in HCC was realized by transcriptionally regulating the expression of human telomerase reverse transcriptase (hTERT). Furthermore, we found that HCC patients with high BPTF expression displayed high hTERT expression, and high BPTF or hTERT expression level was positively correlated with advanced malignancy and poor prognosis in HCC patients. Collectively, our results demonstrate that BPTF promotes HCC growth by targeting hTERT and suggest that the BPTF-hTERT axis maybe a novel and potential therapeutic target in HCC. Keywords: BPTF, hTERT, Hepatocellular carcinoma, Cancer stem cell, Stemness
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- 2019
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6. Prognostic role of tumour-infiltrating lymphocytes assessed by H&E-stained section in gastric cancer: a systematic review and meta-analysis
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Chunfang Tian, Haiyan Jing, Weibo Wang, Yangang Cui, Jianpeng Chen, and Dan Sha
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Medicine - Abstract
Objectives Some studies have identified tumour-infiltrating lymphocytes (TILs) in H&E-stained sections of gastric cancer, but the prognostic and clinicopathological significance of this remains unclear. The objective of this study is to evaluate the associations between H&E-based TIL density and prognosis and clinicopathological characteristics of patients with gastric cancer.Design Systematic review and meta-analysis.Data sources Cochrane Library, PubMed and Embase databases were searched through 25 February 2020.Eligibility criteria Studies evaluating the correlations between TILs assessed by H&E-stained sections and prognosis and clinicopathological characteristics of gastric cancer were included.Data extraction and synthesis Relevant data were extracted and risks of bias were assessed independently by two reviewers. HR and relative risk (RR) with 95% CI were pooled by random-effect models to estimate the associations between TIL density and overall survival (OS) and clinicopathological characteristics, respectively.Results We enrolled nine studies including 2835 cases for the present meta-analysis. High TILs were associated with superior OS (HR=0.68, 95% CI 0.52 to 0.87, p=0.003) compared with low TILs. High TILs were significantly associated with lower depth of invasion (T3–T4 vs T1–T2) (RR=0.58, 95% CI 0.50 to 0.66, p
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- 2021
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7. β-Catenin Cooperates with CREB Binding Protein to Promote the Growth of Tumor Cells
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Wendan Yu, Liren Li, Fufu Zheng, Wenjing Yang, Shilei Zhao, Chunfang Tian, Wenwen Yin, Yiming Chen, Wei Guo, Lijuan Zou, and Wuguo Deng
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Prognosis ,β-catenin ,CBP ,Lung cancer ,Physiology ,QP1-981 ,Biochemistry ,QD415-436 - Abstract
Background/Aims: β-catenin is an integral component of the canonical Wnt signaling pathway, and its mutations are an autosomal recessive cause of colorectal cancer (CRC), medulloblastoma (MDB), and ovarian cancer. Nevertheless, little is known about its function in lung cancers. Methods: We first knocked down β-catenin by siRNA to investigate its effects on lung cancer cell proliferation, migration and apoptosis. Then we verified the interaction between β-catenin and CREB binding protein (CBP) by immunofluoresence and co-immunoprecipition assays. Finally, the expression of β-catenin and CBP in human lung adenocarcinoma specimens were analyzed by immunohistochemistry assay. Results: β-catenin knockdown inhibited cell proliferation, promoted apoptosis and suppressed cell migration in A549 and H460 cells accompanied by the decreased expression of Myc, PCNA, VEGF, CD44, MMP-9, MMP-13 and activated bax/caspase-3 pathway. Furthermore, co-immunoprecipition and immunofluoresence analyses revealed that CBP interacted with β-catenin and contributed to β-catenin-mediated lung cancer cell growth. Abolishment of their interaction by the Wnt/β-catenin inhibitor ICG-001 remarkably suppressed cell proliferation. Immunohistochemistry assay of tissue microarrays from patients with lung cancer indicated that both CBP and β-catenin were highly expressed in tumor tissues and predicted poor prognosis in lung adenocarcinoma patients. Conclusions: Our study has provided new evidence for the role of β-catenin in promoting the growth of lung cancer cells through cooperation with CBP, and suggested that dual targeting of β-catenin and CBP could be a potential therapeutic strategy in lung cancer treatment.
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- 2017
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8. Ku80 promotes melanoma growth and regulates antitumor effect of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway
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Tianze Liu, Lizi Jin, Miao Chen, Zongheng Zheng, Wenjing Lu, Wenhua Fan, Liren Li, Fufu Zheng, Qiaohua Zhu, Huijuan Qiu, Jiani Liu, Manyu Chen, Chunfang Tian, Zheng Hu, Changlin Zhang, Meihua Luo, Jian Li, Tiebang Kang, Lukun Yang, Yizhuo Li, and Wuguo Deng
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Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Melanoma is one of the most malignant and aggressive cancers with high cancer-related deaths. However, it is unclear whether Ku80 regulates tumor growth in human melanoma. In this study, we screened a siRNA library targeting 6024 human genes and identified Ku80 as a potential therapeutic target in melanoma cells. Knockdown of Ku80 significantly suppressed melanoma cell proliferation and induced apoptosis, as well as enhanced the antitumor effect of melatonin in melanoma in vitro and in vivo. Overexpression of Ku80, however, promoted melanoma growth and increased the insensitivity of melanoma cells to melatonin. Mechanistically, we found that Ku80 bound to the PDK1 promoter and activated the transcription of PDK1. Moreover, we showed that the binding of Ku80 at the PDK-1 promoter was HIF1-α dependent, and melatonin degraded HIF1-α in melanoma cells. Furthermore, clinical data revealed that the expression of Ku80 and PDK-1 proteins were positively correlated and elevated in the tumor tissues of melanoma patients, and high expression of Ku80 predicted a poor prognosis in melanoma. Collectively, our study demonstrated that Ku80 promoted melanoma growth and regulated antitumor activity of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway, suggesting that Ku80 may be a potential molecular target for melanoma treatment. Keywords: Ku80, PDK-1, Melatonin, HIF1-α, Melanoma
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- 2019
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9. TRIP4 transcriptionally activates DDIT4 and subsequent mTOR signaling to promote glioma progression
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Xinyu Wan, Sheng Hu, Feng Zhao, Wuguo Deng, Dong Wang, Chunyu Hua, Shilong Han, Ping Guo, Wendan Yu, Wenyang Li, Guoqing Xue, Wei Guo, Chunfang Tian, and Xiaona Lu
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Gene knockdown ,Thyroid hormone receptor ,DDIT4 ,biology ,TOR Serine-Threonine Kinases ,Apoptosis ,Glioma ,medicine.disease ,medicine.disease_cause ,Biochemistry ,Gene Expression Regulation, Neoplastic ,In vivo ,Cell Line, Tumor ,Physiology (medical) ,medicine ,biology.protein ,Cancer research ,Humans ,Tumor promotion ,Carcinogenesis ,PI3K/AKT/mTOR pathway ,Cell Proliferation ,Signal Transduction ,Transcription Factors - Abstract
In spite of significant advances in the understanding of glioma biology and pathology, survival remains poor. Therefore, it is still of great significance to further explore the key factors involved in tumorigenesis and development in glioma and find potential new therapeutic targets. Here, we show that thyroid hormone receptor interactor 4 (TRIP4) is highly expressed in glioma cells and tissues. Patients of glioma with high expression of TRIP4 possess poor overall survival. Knockdown of TRIP4 inhibited tumor cell proliferation, metastasis, and apoptosis suppression, whereas overexpression of TRIP4 displays the opposite effects. Further research showed that TRIP4 promoted glioma progression through regulating DDIT4 expression and subsequent activation of mTOR signaling. DDIT4 overexpression restored the inhibition of tumor growth by TRIP4 knockdown in vitro and in vivo. Consistently, mTOR activity inhibition reversed TRIP4 overexpression-mediated tumor promotion in vitro and in vivo. Moreover, molecular mechanism exploration demonstrates that TRIP4 functions as a specific transcriptional activator to anchor at the promoter region of DDIT4 gene (−196 to −11) to regulate its transcription and such regulation was affected by HIF1α. Clinically, TRIP4 expression is positively correlated with DDIT4 expression in glioma samples based on tissue microarray analysis and both of their high expression predicts the malignancy of the disease. Altogether, our findings identify TRIP4 as a critical promoter of glioma progression by targeting DDIT4 and mTOR signaling successively and suggest that TRIP4-DDIT4 axis has potential to be a novel therapeutic target in glioma treatment.
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- 2021
10. YBX1 mediates autophagy by targeting p110β and decreasing the sensitivity to cisplatin in NSCLC
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Wendan Yu, Yanwei Cui, Tao Guo, Chundong Gu, Taihua Wu, Qiang Xie, Manyu Chen, Lei Zhao, Fengzhou Li, Shilei Zhao, Chunfang Tian, Jiaojiao Hao, Sheng Hu, Zhuoshi Li, Lei Fang, and Ping Guo
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Male ,Cancer Research ,Lung Neoplasms ,Immunology ,Mice, Nude ,Apoptosis ,Article ,Cellular and Molecular Neuroscience ,In vivo ,Carcinoma, Non-Small-Cell Lung ,Cell Line, Tumor ,Macroautophagy ,Autophagy ,Carcinoma ,Animals ,Humans ,Medicine ,lcsh:QH573-671 ,neoplasms ,Aged ,Cell Proliferation ,Aged, 80 and over ,Cisplatin ,Mice, Inbred BALB C ,Gene knockdown ,business.industry ,lcsh:Cytology ,Cell Biology ,Middle Aged ,medicine.disease ,respiratory tract diseases ,Class Ia Phosphatidylinositol 3-Kinase ,Disease Models, Animal ,Cell culture ,Cancer research ,Beclin-1 ,Female ,Y-Box-Binding Protein 1 ,Lung cancer ,Signal transduction ,business ,Microtubule-Associated Proteins ,medicine.drug - Abstract
Y-box binding protein 1 (YBX1) is involved in the development of multiple types of tumors. However, the relationship between YBX1 and autophagy in non-small cell lung cancer (NSCLC) remains unclear. In this study, we analyzed the expression and clinical significance of YBX1 and markers of autophagy (LC3I/II) in NSCLC and examined their roles in regulating sensitivity to cisplatin in NSCLC. The retrospective analysis of patients with NSCLC indicated that YBX1 was positively correlated with autophagy. Increased levels of YBX1 or autophagy also observed in NSCLC cells compared with those in 16HBE cells. Compared to the controls, the knockdown of YBX1 expression suppressed autophagy, increased drug sensitivity and promoted apoptosis in response to cisplatin in NSCLC cells by targeting the p110β promoter and inhibiting p110β/Vps34/beclin1 signaling pathways. We also demonstrated in an in vivo study that the overexpressed YBX1 effectively increased NSCLC growth and progression and decreased the sensitivity to cisplatin by inducing autophagy in a xenograft tumor model, and these effects were concomitant with the increasing of p110β and beclin1 expression. Collectively, these results show that YBX1 plays an essential role in autophagy in NSCLC.
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- 2020
11. The effect characteristics of temperature on stroke mortality in Inner Mongolia and globally
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Liqun Gao, Hongwei Li, Zhihui Hao, Ruijie Wu, Dejun Sun, Chao Dong, Maolin Du, Wenfang Guo, Xiaoling Sun, Di Yu, Juan Sun, Rina Wu, Mingzhu Niu, Chunfang Tian, and Nengjun Zhao
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Male ,030203 arthritis & rheumatology ,China ,Atmospheric Science ,010504 meteorology & atmospheric sciences ,Ecology ,Health, Toxicology and Mutagenesis ,Diurnal temperature variation ,Temperature ,Time lag ,Middle Aged ,Stroke mortality ,Biology ,Inner mongolia ,01 natural sciences ,Latitude ,Stroke ,03 medical and health sciences ,0302 clinical medicine ,Humans ,Female ,cardiovascular diseases ,Stroke incidence ,0105 earth and related environmental sciences ,Demography - Abstract
The current study investigated the correlation between stroke mortality and temperature. Monthly and seasonal variations in stroke mortality were plotted and daily stroke-related deaths were calculated. The lag times were calculated using the time series analysis. The correlation between stroke incidence and the diurnal temperature range (DTR) was analyzed using case-crossover analysis. Global stroke mortality was described in five latitudes. In the eastern region of Inner Mongolia, the stroke mortality was 174.18/105, about twice of that of the midwestern regions (87.07/105), and temperature was negatively correlated with stroke mortality. Mortality peaked in the winter and troughed in the summer (χ2 = 13.634, P 40°; the highest mortality was 188.05/105 at the highest latitude. Only in relatively cold regions as the temperature decreases does stroke mortality increase for various populations. Differences in the time lag as well as in the DTR lag and DTR critical point vary for both the temperature and region.
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- 2018
12. CRSP8 promotes thyroid cancer progression by antagonizing IKKα-induced cell differentiation
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Sheng Hu, Changlin Zhang, Jiaojiao Hao, Lijuan Zou, Kun Zou, Wuguo Deng, Miao Chen, Wenyang Li, Manyu Chen, Fangyun Xie, Qian Long, Yizhuo Li, Ruozhu Wang, Yina Liao, Ping Guo, Yao Sun, Wei Guo, Yijun Hua, Silei Sui, Yan Zuo, Chunfang Tian, Xiaonan Wang, and Wendan Yu
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0301 basic medicine ,Male ,Cellular differentiation ,Mice, Nude ,Antineoplastic Agents ,Apoptosis ,Biology ,Thyroid Carcinoma, Anaplastic ,Article ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Thyroid Neoplasms ,Anaplastic thyroid cancer ,Molecular Biology ,Thyroid cancer ,Cell Proliferation ,Epirubicin ,Regulation of gene expression ,Gene knockdown ,Mice, Inbred BALB C ,Mediator Complex ,Cell growth ,Cell Differentiation ,Cell Biology ,Oncogenes ,medicine.disease ,Xenograft Model Antitumor Assays ,I-kappa B Kinase ,Gene regulation ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Drug Resistance, Neoplasm ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Cisplatin ,Signal Transduction - Abstract
CRSP8 plays an important role in recruiting mediators to genes through direct interaction with various DNA-bound transactivators. In this study, we uncovered the unique function of CRSP8 in suppressing thyroid cancer differentiation and promoting thyroid cancer progression via targeting IKKα signaling. CRSP8 was highly expressed in human thyroid cancer cells and tissues, especially in anaplastic thyroid cancer (ATC). Knockdown of CRSP8 suppressed cell growth, migration, invasion, stemness, and induced apoptosis and differentiation in ATC cells, while its overexpression displayed opposite effects in differentiated thyroid cancer (DTC) cells. Mechanistically, CRSP8 downregulated IKKα expression by binding to the IKKα promoter region (−257 to −143) to negatively regulate its transcription. Knockdown or overexpression of IKKα significantly reversed the expression changes of the differentiation and EMT-related markers and cell growth changes mediated by CRSP8 knockdown or overexpression in ATC or DTC cells. The in vivo study also validated that CRSP8 knockdown inhibited the growth of thyroid cancer by upregulating IKKα signaling in a mouse model of human ATC. Furthermore, we found that CRSP8 regulated the sensitivity of thyroid cancer cells to chemotherapeutics, including cisplatin and epirubicin. Collectively, our results demonstrated that CRSP8 functioned as a modulator of IKKα signaling and a suppressor of thyroid cancer differentiation, suggesting a potential therapeutic strategy for ATC by targeting CRSP8/IKKα pathway.
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- 2020
13. BPTF promotes hepatocellular carcinoma growth by modulating hTERT signaling and cancer stem cell traits
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Xinrui Zhao, Lizhi Zhang, Qian Yang, Yina Liao, Manyu Chen, Changlin Zhang, Wendan Yu, Tianhua Zhu, Fufu Zheng, Yizhuo Li, Wei Guo, Lijuan Zou, Chaoliang Diao, Zhipeng Tang, Wuguo Deng, Miao Chen, Ping Guo, Chunfang Tian, Jiaojiao Hao, and Sheng Hu
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0301 basic medicine ,Male ,Hepatocellular carcinoma ,Clinical Biochemistry ,Gene Expression ,Biochemistry ,Metastasis ,Mice ,0302 clinical medicine ,Cell Movement ,Stemness ,Cell Self Renewal ,Neoplasm Metastasis ,lcsh:QH301-705.5 ,Telomerase ,Cells, Cultured ,Gene knockdown ,lcsh:R5-920 ,Liver Neoplasms ,Antigens, Nuclear ,Prognosis ,Immunohistochemistry ,Gene Knockdown Techniques ,Neoplastic Stem Cells ,BPTF ,lcsh:Medicine (General) ,hTERT ,Research Paper ,Signal Transduction ,Carcinoma, Hepatocellular ,Antineoplastic Agents ,Nerve Tissue Proteins ,Biology ,Chromatin remodeling ,03 medical and health sciences ,Cancer stem cell ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Telomerase reverse transcriptase ,Transcription factor ,neoplasms ,Cell Proliferation ,Cell growth ,Organic Chemistry ,medicine.disease ,Xenograft Model Antitumor Assays ,digestive system diseases ,Bromodomain ,Disease Models, Animal ,030104 developmental biology ,lcsh:Biology (General) ,Drug Resistance, Neoplasm ,Cancer research ,030217 neurology & neurosurgery ,Biomarkers ,Transcription Factors - Abstract
Bromodomain PHD finger transcription factor (BPTF), a core subunit of nucleosome-remodeling factor (NURF) complex, plays an important role in chromatin remodeling. However, its precise function and molecular mechanism involved in hepatocellular carcinoma (HCC) growth are still poorly defined. Here, we demonstrated the tumor-promoting role of BPTF in HCC progression. BPTF was highly expressed in HCC cells and tumor tissues of HCC patients compared with normal liver cells and tissues. Knockdown of BPTF inhibited cell proliferation, colony formation and stem cell-like traits in HCC cells. In addition, BPTF knockdown effectively sensitized the anti-tumor effect of chemotherapeutic drugs and induced more apoptosis in HCC cells. Consistently, knockdown of BPTF in a xenograft mouse model also suppressed tumor growth and metastasis accompanied by the suppression of cancer stem cells (CSC)-related protein markers. Moreover, the mechanism study showed that the tumor-promoting role of BPTF in HCC was realized by transcriptionally regulating the expression of human telomerase reverse transcriptase (hTERT). Furthermore, we found that HCC patients with high BPTF expression displayed high hTERT expression, and high BPTF or hTERT expression level was positively correlated with advanced malignancy and poor prognosis in HCC patients. Collectively, our results demonstrate that BPTF promotes HCC growth by targeting hTERT and suggest that the BPTF-hTERT axis maybe a novel and potential therapeutic target in HCC. Keywords: BPTF, hTERT, Hepatocellular carcinoma, Cancer stem cell, Stemness
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- 2018
14. β-Catenin Cooperates with CREB Binding Protein to Promote the Growth of Tumor Cells
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Wenjing Yang, Wenwen Yin, Shilei Zhao, Lijuan Zou, Yiming Chen, Chunfang Tian, Wendan Yu, Liren Li, Wei Guo, Wuguo Deng, and Fufu Zheng
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Male ,Vascular Endothelial Growth Factor A ,0301 basic medicine ,Lung Neoplasms ,Physiology ,Apoptosis ,Kaplan-Meier Estimate ,lcsh:Physiology ,0302 clinical medicine ,Cell Movement ,lcsh:QD415-436 ,RNA, Small Interfering ,Wnt Signaling Pathway ,beta Catenin ,bcl-2-Associated X Protein ,lcsh:QP1-981 ,biology ,Caspase 3 ,Wnt signaling pathway ,Middle Aged ,Prognosis ,CREB-Binding Protein ,Immunohistochemistry ,Matrix Metalloproteinase 9 ,Proto-Oncogene Proteins c-bcl-2 ,030220 oncology & carcinogenesis ,Adenocarcinoma ,Female ,RNA Interference ,Lung cancer ,Beta-catenin ,Pyrimidinones ,CBP ,lcsh:Biochemistry ,03 medical and health sciences ,Cell Line, Tumor ,Matrix Metalloproteinase 13 ,medicine ,Humans ,CREB-binding protein ,Aged ,Cell Proliferation ,Neoplasm Staging ,Cell growth ,CD44 ,β-catenin ,Bridged Bicyclo Compounds, Heterocyclic ,medicine.disease ,030104 developmental biology ,Microscopy, Fluorescence ,A549 Cells ,Catenin ,biology.protein ,Cancer research - Abstract
Background/Aims: β-catenin is an integral component of the canonical Wnt signaling pathway, and its mutations are an autosomal recessive cause of colorectal cancer (CRC), medulloblastoma (MDB), and ovarian cancer. Nevertheless, little is known about its function in lung cancers. Methods: We first knocked down β-catenin by siRNA to investigate its effects on lung cancer cell proliferation, migration and apoptosis. Then we verified the interaction between β-catenin and CREB binding protein (CBP) by immunofluoresence and co-immunoprecipition assays. Finally, the expression of β-catenin and CBP in human lung adenocarcinoma specimens were analyzed by immunohistochemistry assay. Results: β-catenin knockdown inhibited cell proliferation, promoted apoptosis and suppressed cell migration in A549 and H460 cells accompanied by the decreased expression of Myc, PCNA, VEGF, CD44, MMP-9, MMP-13 and activated bax/caspase-3 pathway. Furthermore, co-immunoprecipition and immunofluoresence analyses revealed that CBP interacted with β-catenin and contributed to β-catenin-mediated lung cancer cell growth. Abolishment of their interaction by the Wnt/β-catenin inhibitor ICG-001 remarkably suppressed cell proliferation. Immunohistochemistry assay of tissue microarrays from patients with lung cancer indicated that both CBP and β-catenin were highly expressed in tumor tissues and predicted poor prognosis in lung adenocarcinoma patients. Conclusions: Our study has provided new evidence for the role of β-catenin in promoting the growth of lung cancer cells through cooperation with CBP, and suggested that dual targeting of β-catenin and CBP could be a potential therapeutic strategy in lung cancer treatment.
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- 2017
15. Melatonin synergizes BRAF-targeting agent vemurafenib in melanoma treatment by inhibiting iNOS/hTERT signaling and cancer-stem cell traits
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Wenhua Fan, Changlin Zhang, Lijuan Zou, Jiaojiao Hao, Ge Qin, Liren Li, Chunfang Tian, Qian Yang, Miao Chen, Chaoliang Diao, Wuguo Deng, Lijun Qin, Yandong Ren, Penghui Zhou, Manyu Chen, Sheng Hu, Yizhuo Li, Xiuping Zhang, Qian Long, Kui Jiang, Ping Guo, Ranran Tang, Wendan Yu, Tianhua Zhu, Jingshu Wang, and Wei Guo
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Male ,0301 basic medicine ,Cancer Research ,Skin Neoplasms ,Nude ,Cell ,Nitric Oxide Synthase Type II ,Apoptosis ,Antioxidants ,NF-κB ,Mice ,0302 clinical medicine ,Antineoplastic Combined Chemotherapy Protocols ,Vemurafenib ,Melanoma ,Telomerase ,Cancer ,Melatonin ,Tumor ,biology ,Chemistry ,NF-kappa B ,Drug Synergism ,Cell cycle ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,iNOS ,medicine.anatomical_structure ,Oncology ,5.1 Pharmaceuticals ,030220 oncology & carcinogenesis ,Neoplastic Stem Cells ,Development of treatments and therapeutic interventions ,hTERT ,Biotechnology ,Signal Transduction ,medicine.drug ,Proto-Oncogene Proteins B-raf ,Epithelial-Mesenchymal Transition ,Oncology and Carcinogenesis ,Mice, Nude ,Antineoplastic Agents ,lcsh:RC254-282 ,Cell Line ,03 medical and health sciences ,Cancer stem cell ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Oncology & Carcinogenesis ,Protein Kinase Inhibitors ,neoplasms ,Cell growth ,Research ,CD44 ,Cell Cycle Checkpoints ,medicine.disease ,Xenograft Model Antitumor Assays ,030104 developmental biology ,biology.protein ,Cancer research - Abstract
Background As the selective inhibitor of BRAF kinase, vemurafenib exhibits effective antitumor activities in patients with V600 BRAF mutant melanomas. However, acquired drug resistance invariably develops after its initial treatment. Methods Immunohistochemical staining was performed to detect the expression of iNOS and hTERT, p-p65, Epcam, CD44, PCNA in mice with melanoma xenografts. The proliferation and migration of melanoma cells were detected by MTT, tumorsphere culture, cell cycle, cell apoptosis, AO/EB assay and colony formation, transwell assay and scratch assay in vitro, and tumor growth differences were observed in xenograft nude mice. Changes in the expression of key molecules in the iNOS/hTERT signaling pathways were detected by western blot. Nucleus-cytoplasm separation, and immunofluorescence analyses were conducted to explore the location of p50/p65 in melanoma cell lines. Flow cytometry assay were performed to determine the expression of CD44. Pull down assay and ChIP assay were performed to detect the binding ability of p65 at iNOS and hTERT promoters. Additionally, hTERT promoter-driven luciferase plasmids were transfected in to melanoma cells with indicated treatment to determine luciferase activity of hTERT. Results Melatonin significantly and synergistically enhanced vemurafenib-mediated inhibitions of proliferation, colony formation, migration and invasion and promoted vemurafenib-induced apoptosis, cell cycle arresting and stemness weakening in melanoma cells. Further mechanism study revealed that melatonin enhanced the antitumor effect of vemurafenib by abrogating nucleus translocation of NF-κB p50/p65 and their binding at iNOS and hTERT promoters, thereby suppressing the expression of iNOS and hTERT. The elevated anti-tumor capacity of vemurafenib upon co-treatment with melatonin was also evaluated and confirmed in mice with melanoma xenografts. Conclusions Collectively, our results demonstrate melatonin synergizes the antitumor effect of vemurafenib in human melanoma by inhibiting cell proliferation and cancer-stem cell traits via targeting NF-κB/iNOS/hTERT signaling pathway, and suggest the potential of melatonin in antagonizing the toxicity of vemurafenib and augmenting its sensitivities in melanoma treatment. Electronic supplementary material The online version of this article (10.1186/s13046-019-1036-z) contains supplementary material, which is available to authorized users.
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- 2019
16. Cleavage and polyadenylation specific factor 4 promotes colon cancer progression by transcriptionally activating hTERT
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Jinjin Pan, Wenhua Fan, Chaoliang Diao, Wenyang Li, Wendan Yu, Yan Zuo, Yao Sun, Xiaojun Wu, Ping Guo, Qian Yang, Liren Li, Tianhua Zhu, Sheng Hu, Jiaojiao Hao, Wuguo Deng, Congcong Liu, Ruozhu Wang, Manyu Chen, Chunfang Tian, Wei Guo, Yizhuo Li, Shiyong Lin, and Zongheng Zheng
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0301 basic medicine ,Male ,Polyadenylation ,Colorectal cancer ,Cell Survival ,Mice, Nude ,Biology ,03 medical and health sciences ,Mice ,0302 clinical medicine ,In vivo ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Telomerase reverse transcriptase ,Genetic Predisposition to Disease ,Lung cancer ,Promoter Regions, Genetic ,Molecular Biology ,Telomerase ,mRNA Cleavage and Polyadenylation Factors ,Gene knockdown ,Mice, Inbred BALB C ,Cell growth ,Cell Cycle ,Cleavage And Polyadenylation Specificity Factor ,Cell Biology ,Cell Cycle Checkpoints ,medicine.disease ,In vitro ,Peptide Fragments ,Gene Expression Regulation, Neoplastic ,Disease Models, Animal ,030104 developmental biology ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,Colonic Neoplasms ,Cancer research ,Disease Progression - Abstract
CPSF4 was identified as a crucial tumorigenic factor in lung cancer development. However, its precise function and the underlying molecular mechanisms in colon cancer progression remain completely unknown. Here, we demonstrate CPSF4 was highly expressed in human colon cancer cells and tissues. Its knockdown inhibited colorectal cancer progression in vitro, including cell proliferation, migration, invasion and stemness maintenance. In contrast, the ectopic overexpression of CPSF4 had the opposite effects in vitro and in vivo. Further mechanistic studies demonstrated that CPSF4 facilitated colorectal tumorigenesis and development partially through transcriptionally regulating hTERT expression by cooperating with NF-kB1 and co-anchoring at hTERT promoter -321 to -234 fragment. In addition, clinical samples analysis indicated that CPSF4 expression was positively correlated with hTERT, and the simultaneously high expression of CPSF4 and hTERT predicted poor patient outcome. Overall, our findings established CPSF4 as a pro-tumorigenic factor in colorectal cancer progression, and suggested that targeting CPSF4-hTERT axis may represent a promising therapeutic strategy in colon cancer treatment.
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- 2019
17. Additional file 1: of Melatonin synergizes BRAF-targeting agent vemurafenib in melanoma treatment by inhibiting iNOS/hTERT signaling and cancer-stem cell traits
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Jiaojiao Hao, Wenhua Fan, Yizhuo Li, Ranran Tang, Chunfang Tian, Yang, Qian, Tianhua Zhu, Chaoliang Diao, Hu, Sheng, Manyu Chen, Guo, Ping, Long, Qian, Changlin Zhang, Qin, Ge, Wendan Yu, Chen, Miao, Liren Li, Lijun Qin, Jingshu Wang, Xiuping Zhang, Yandong Ren, Penghui Zhou, Lijuan Zou, Jiang, Kui, Guo, Wei, and Wuguo Deng
- Abstract
Figure S1. Melatonin enhanced the inhibition of cell proliferation by vemurafenib. (A). BRAF V600E, p-ERK and ERK was respectively detected by Western blot assay in melanoma cells (A375, SK-mel-28, G361 and A431). (B). ABCG2 was respectively detected by Western blot assay in A375 and A375R cells. (C). Human melanoma cells (A375R) were treated with the increasing doses of vemurafenib (VE), melatonin (MT) alone or their combination for 48 h, and the cell viability was examined by MTT assay. (D). The IC50 values of vemurafenib (VE) for cell viability inhibition in A375R cells treated with or without melatonin (MT) were determined. Figure S2. Melatonin enhanced the inhibition of cell migration and invasion by vemurafenib (A). Cell migration was analyzed by a scratch assay. A375R cells were treated with vemurafenib (VE) (4 μM), melatonin (MT) (1.0 mM) or their combination. After 36 h, the wound gap was observed and photographed, and the distance of migration cells were calculated relative to the original gap. (B). Cell invasion was analyzed by a transwell assay in A375R cells with different treatment. The invaded cells were stained and observed, and the number of the invasion cells was presented. The data is presented as mean ± SD of three separate experiments, *P
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- 2019
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18. Effects of occupation on intracerebral hemorrhage-related deaths in Inner Mongolia
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Ying Yang, Qingxia Wang, Nan Zhang, Wenting Chen, Maolin Du, Chao Dong, Chunfang Tian, Lehui Li, Neng Jun Zhao, Han Bao, Liqun Gao, Xiaoling Sun, Jiayi Li, Huiqiu Zheng, Li Wei Niu, Juan Sun, Yan Liu, and Baofeng Chi
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Male ,Risk ,China ,Health, Toxicology and Mutagenesis ,education ,Inner mongolia ,Logistic regression ,Occupational safety and health ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,medicine ,Humans ,0501 psychology and cognitive sciences ,Occupations ,Mortality ,050107 human factors ,Cerebral Hemorrhage ,Intracerebral hemorrhage ,Marital Status ,Occupational health ,business.industry ,Mortality rate ,05 social sciences ,Public Health, Environmental and Occupational Health ,Odds ratio ,Middle Aged ,medicine.disease ,030210 environmental & occupational health ,Inner Mongolia ,Case-Control Studies ,Marital status ,Female ,Original Article ,business ,Demography - Abstract
This study assessed the relationship between occupation and Intracerebral Hemorrhage-related deaths and compared the differences in ICH-related deaths rates between the eastern and midwestern regions of Inner Mongolia. We used the case-control method. Cases included Intracerebral Hemorrhage-related deaths that occurred from 2009 to 2012 in Inner Mongolia while controls included non-circulatory system disease deaths that occurred during the same period. Odds ratios (ORs) for Intracerebral Hemorrhage-related deaths were calculated using logistic regression analysis, estimated according to occupation, and adjusted for marital status and age. The Intracerebral Hemorrhage mortality rate in the eastern regions (125.19/100000) was nearly 3 times higher than that in the midwestern regions (45.31/100000). ORs for agriculture-livestock workers, service professionals and general workers, professional workers and senior officials were in descending order. The age-adjusted OR for Intracerebral Hemorrhage-related deaths was lowest in unmarried men senior officials (OR 0.37, 95% CI 0.14-0.99). The Intracerebral Hemorrhage mortality rate in the eastern regions was much higher than that of the midwestern regions, since about 90% of Intracerebral Hemorrhage-related deaths in the eastern regions were those of agriculture-livestock workers who has the largest labor intensity of any other occupation assessed.
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- 2018
19. Ku80 promotes melanoma growth and regulates antitumor effect of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway
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Miao Chen, Wuguo Deng, Fufu Zheng, Zheng Hu, Changlin Zhang, Huijuan Qiu, Wenhua Fan, Tianze Liu, Tiebang Kang, Chunfang Tian, Zongheng Zheng, Lukun Yang, Jian Li, Meihua Luo, Qiaohua Zhu, Jiani Liu, Wenjing Lu, Liren Li, Lizi Jin, Manyu Chen, and Yizhuo Li
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Male ,0301 basic medicine ,Ku80 ,Transcription, Genetic ,Clinical Biochemistry ,Apoptosis ,Biochemistry ,0302 clinical medicine ,RNA, Small Interfering ,Promoter Regions, Genetic ,lcsh:QH301-705.5 ,Melanoma ,Melatonin ,lcsh:R5-920 ,Gene knockdown ,Chemistry ,PDK-1 ,Middle Aged ,Prognosis ,Female ,Signal transduction ,lcsh:Medicine (General) ,Protein Binding ,Signal Transduction ,medicine.drug ,HIF1-α ,Cell Survival ,Mice, Nude ,Antineoplastic Agents ,Models, Biological ,Article ,03 medical and health sciences ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Ku Autoantigen ,neoplasms ,Cell Proliferation ,Cell growth ,Organic Chemistry ,Pyruvate Dehydrogenase Acetyl-Transferring Kinase ,Hypoxia-Inducible Factor 1, alpha Subunit ,medicine.disease ,In vitro ,030104 developmental biology ,lcsh:Biology (General) ,Cancer research ,030217 neurology & neurosurgery - Abstract
Melanoma is one of the most malignant and aggressive cancers with high cancer-related deaths. However, it is unclear whether Ku80 regulates tumor growth in human melanoma. In this study, we screened a siRNA library targeting 6024 human genes and identified Ku80 as a potential therapeutic target in melanoma cells. Knockdown of Ku80 significantly suppressed melanoma cell proliferation and induced apoptosis, as well as enhanced the antitumor effect of melatonin in melanoma in vitro and in vivo. Overexpression of Ku80, however, promoted melanoma growth and increased the insensitivity of melanoma cells to melatonin. Mechanistically, we found that Ku80 bound to the PDK1 promoter and activated the transcription of PDK1. Moreover, we showed that the binding of Ku80 at the PDK-1 promoter was HIF1-α dependent, and melatonin degraded HIF1-α in melanoma cells. Furthermore, clinical data revealed that the expression of Ku80 and PDK-1 proteins were positively correlated and elevated in the tumor tissues of melanoma patients, and high expression of Ku80 predicted a poor prognosis in melanoma. Collectively, our study demonstrated that Ku80 promoted melanoma growth and regulated antitumor activity of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway, suggesting that Ku80 may be a potential molecular target for melanoma treatment. Keywords: Ku80, PDK-1, Melatonin, HIF1-α, Melanoma
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- 2019
20. Effects of occupation on intracerebral hemorrhage-related deaths in Inner Mongolia.
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Liqun GAO, Maolin DU, Jiayi LI, Neng jun ZHAO, Ying YANG, Chao DONG, Xiao ling SUN, Baofeng CHI, Qingxia WANG, Wenting CHEN, Chunfang TIAN, Nan ZHANG, Lehui LI, Li wei NIU, Huiqiu ZHENG, Han BAO, Yan LIU, and Juan SUN
- Abstract
This study assessed the relationship between occupation and Intracerebral Hemorrhagerelated deaths and compared the differences in ICH-related deaths rates between the eastern and midwestern regions of Inner Mongolia. We used the case-control method. Cases included Intracerebral Hemorrhage-related deaths that occurred from 2009 to 2012 in Inner Mongolia while controls included non-circulatory system disease deaths that occurred during the same period. Odds ratios (ORs) for Intracerebral Hemorrhage-related deaths were calculated using logistic regression analysis, estimated according to occupation, and adjusted for marital status and age. The Intracerebral Hemorrhage mortality rate in the eastern regions (125.19/100000) was nearly 3 times higher than that in the midwestern regions (45.31/100000). ORs for agriculture-livestock workers, service professionals and general workers, professional workers and senior officials were in descending order. The age-adjusted OR for Intracerebral Hemorrhage-related deaths was lowest in unmarried men senior officials (OR 0.37, 95% CI 0.14-0.99). The Intracerebral Hemorrhage mortality rate in the eastern regions was much higher than that of the midwestern regions, since about 90% of Intracerebral Hemorrhage-related deaths in the eastern regions were those of agriculture-livestock workers who has the largest labor intensity of any other occupation assessed. [ABSTRACT FROM AUTHOR]
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- 2019
- Full Text
- View/download PDF
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