15 results on '"Yigang Qian"'
Search Results
2. Clinical prediction score for superficial surgical site infections: Real‐life data from a retrospective single‐centre analysis of 812 hepatectomies
- Author
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Bei Wang, Zuowei Ni, Yigang Qian, Juwei Shen, and Shusen Zheng
- Subjects
Adult ,Male ,China ,medicine.medical_specialty ,Blood transfusion ,Multivariate analysis ,medicine.medical_treatment ,Dermatology ,Risk Assessment ,law.invention ,030207 dermatology & venereal diseases ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,law ,Clinical Decision Rules ,Internal medicine ,medicine ,Hepatectomy ,Humans ,Surgical Wound Infection ,030212 general & internal medicine ,Aged ,Retrospective Studies ,Aged, 80 and over ,Framingham Risk Score ,Receiver operating characteristic ,business.industry ,Liver Neoplasms ,Original Articles ,Perioperative ,Middle Aged ,Intensive care unit ,Confidence interval ,ROC Curve ,Multivariate Analysis ,Female ,Surgery ,business - Abstract
Superficial surgical site infections (SSIs) are one of the most common postoperative complications of hepatectomy for liver cancer. The objective of this study is to clarify the risk factors and determine a clinical prediction score for SSIs after partial hepatectomy for malignant tumour. A total of 812 consecutive patients were enrolled who underwent partial hepatectomy for liver malignant tumour from January 2017 to December 2017. Univariate and multivariate analyses were conducted to identify the risk factors for SSIs. Clinical prediction score was then constructed using coefficients of identified significant predictors. Risk stratification was then carried out by receiver operating characteristic curve analysis. Of all the 812 patients, SSIs were observed in 31 (3.82%) patients. A multivariate analysis identified four predictors as independent risk factors for SSIs, which were splenomegaly, perioperative blood transfusion, intensive care unit (ICU) admission, and low postoperative serum albumin concentration (
- Published
- 2019
3. LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R
- Author
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Jie Zhou, Zhou Ye, Zhen Lv, Shusen Zheng, Weilin Wang, Yigang Qian, Hai-Yong Chen, Ai-Bin Zhang, and Le Fan
- Subjects
Adult ,Male ,0301 basic medicine ,Pancreatic cancer cells ,Physiology ,Proliferation ,GLP1R gene ,Apoptosis ,CAMP/PKA signaling pathway ,CREB ,Second Messenger Systems ,Glucagon-Like Peptide-1 Receptor ,lcsh:Physiology ,Flow cytometry ,lcsh:Biochemistry ,03 medical and health sciences ,Invasion ,Cell Movement ,Annexin ,Pancreatic cancer ,Cyclic AMP ,medicine ,Humans ,Neoplasm Invasiveness ,lcsh:QD415-436 ,RNA, Neoplasm ,Migration ,Aged ,Cell Proliferation ,Aged, 80 and over ,lcsh:QP1-981 ,biology ,medicine.diagnostic_test ,Cell growth ,Chemistry ,Microarray analysis techniques ,Middle Aged ,Linc01121 ,medicine.disease ,Cyclic AMP-Dependent Protein Kinases ,Neoplasm Proteins ,Pancreatic Neoplasms ,030104 developmental biology ,Real-time polymerase chain reaction ,Cancer research ,biology.protein ,Female ,RNA, Long Noncoding - Abstract
Background/Aims: Pancreatic cancer is an aggressive malignancy as a result of highly metastatic potential. The current study was carried out to alter the expression of LINC01121 in pancreatic cancer, with the aim of elucidating its effects on the biological processes of cell proliferation, migration, invasion, and apoptosis. We hypothesized that both the GLP1R gene and cAMP/PKA signaling pathway participate in the aforementioned process. Methods: Microarray data (GSE14245, GSE27890 and GSE16515) and annotating probe files linked to pancreatic cancer were downloaded through the GEO database. The Multi Experiment Matrix (MEM) site was used to predict the target gene of lncRNA. Both pancreatic cancer tissues (n = 56) and paracancerous tissues (n = 45) were collected from patients diagnosed with pancreatic cancer. Immunohistochemistry was applied to identify the positive expression rate of GLP1R protein. Isolated pancreatic cancer cells and PANC-1 cells were independently classified into the blank, negative control (NC), LINC01121 vector, siRNA-LINC01121, siRNA-GLP1R and siRNA-LINC01121 + siRNA-GLP1R groups. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis were applied to detect the expressions of LINC01121, GLP1R, cAMP, PKA, CREB, Bcl-2, Bad and PCNA. Cell proliferation, migration, invasion, cycle progression, and apoptosis were examined by MTT assay, scratch test, Transwell assay and flow cytometry analyses of Annexin V-FITC/PI staining. Results: Observations were made indicating that LINC01121 was highly expressed, while low expressions of GLP1R in pancreatic cancer were detected based on microarray data, which was largely in consistent with the data collected of LINC01121 and GLP1R within the tissues. The target prediction program and luciferase activity analysis was testament to the notion suggesting that GLP1R was indeed a target of LINC01121. In contrast to the blank and NC groups, the LINC01121 vector group exhibited increased expressions of LINC01121; decreased mRNA and protein levels of GLP1R, Bad, cAMP, and PKA; increased protein levels of CREB, Bcl-2, PCNA, p-PKA and p-CREB; increased cell proliferation, migration and invasion; and decreased cell apoptosis. There was no significant difference detected among the blank, NC, and siRNA-LINC01121 + siRNA-GLP1R groups, except that decreased LINC01121 expression was determined in the siRNA-LINC01121 + siRNA-GLP1R group. Parallel data were observed in the pancreatic cancer cells and PANC-1 cells. Conclusion: The current study presents evidence indicating that LINC01121 might inhibit apoptosis while acting to promote proliferation, migration, and invasion of pancreatic cancer cells, supplementing the stance held that LINC01121 functions as a tumor promoter by means of its involvement in the process of translational repression of the GLP1R and inhibition of the cAMP/PKA signaling pathway.
- Published
- 2018
4. Cancer-associated fibroblasts promote M2 polarization of macrophages in pancreatic ductal adenocarcinoma
- Author
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Haiyang Xie, Ai-Bin Zhang, Lin Zhou, Zhou Ye, Yigang Qian, Shusen Zheng, Yan Shen, and Hai-Yong Chen
- Subjects
0301 basic medicine ,Cancer Research ,tumor‐associated macrophages ,0302 clinical medicine ,Cancer-Associated Fibroblasts ,Cell Movement ,Pancreatic tumor ,Tumor Cells, Cultured ,Tumor Microenvironment ,Original Research ,Cancer Biology ,reactive oxygen species ,Chemistry ,Cell Polarity ,Gene Expression Regulation, Neoplastic ,Oncology ,030220 oncology & carcinogenesis ,medicine.symptom ,Mannose Receptor ,Carcinoma, Pancreatic Ductal ,Macrophage colony-stimulating factor ,medicine.medical_specialty ,Stromal cell ,Antigens, Differentiation, Myelomonocytic ,Receptors, Cell Surface ,Macrophage colony‐stimulating factor (M‐CSF) ,Cancer‐associated fibroblasts ,03 medical and health sciences ,Antigens, CD ,Cell Line, Tumor ,Internal medicine ,pancreatic adenocarcinoma ,medicine ,Humans ,Lectins, C-Type ,Radiology, Nuclear Medicine and imaging ,Cell Proliferation ,Tumor microenvironment ,Cell growth ,Macrophage Colony-Stimulating Factor ,Macrophages ,medicine.disease ,Coculture Techniques ,Desmoplasia ,Pancreatic Neoplasms ,Mannose-Binding Lectins ,030104 developmental biology ,Endocrinology ,Culture Media, Conditioned ,Cancer research ,CD163 - Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by remarkable desmoplasia with infiltration of distinct cellular components. Cancer‐associated fibroblasts (CAFs) has been shown to be among the most prominent cells and played a significant role in shaping the tumor microenvironment by interacting with other type of cells. Here, we aimed to investigate the effect of CAFs in modulating phenotype of tumor‐associated macrophages (TAM). Under treatment of CAFs conditioned medium (CM) or direct co‐culture with CAFs, monocytes exhibited enhanced expression of CD206 and CD163 compared with control group (P
- Published
- 2017
5. Mutational landscape of AKT1/2/3 in Chinese patients with solid tumors
- Author
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Qiuyue Pan, Songfeng Yu, Qi Ling, Feng Xiao Chen, Yongzhong Wei, Shiyun Cui, Weijia Fang, Hui Kong, Xiaofeng Tang, Lin Zhang, Shiyue Zhang, Liang Xue, Lingxiang Liu, Min Xiao, Yigang Qian, Juming Li, Haibo Mou, Juan Du, Jia Wei, and Ting Wang
- Subjects
Cancer Research ,Oncology ,business.industry ,Cancer research ,AKT1 ,Medicine ,Akt inhibitor ,business ,Protein kinase B ,PI3K/AKT/mTOR pathway - Abstract
e15566 Background: As a central component of PI3K/AKT pathway, AKT serves as an attractive target of anti-cancer strategy with various AKT inhibitors, which show great promise in phase I/II clinical trials. This study aimed to investigate AKT1/2/3 status in different types of cancers by using next generation sequencing (NGS). Methods: Formalin-fixed, paraffin-embedded (FFPE) tumor samples were collected from 10,010 Chinese patients with solid tumors and subjected to next-generation sequencing (NGS)-based 450 gene panel testing carried out by a College of American Pathologists (CAP) accredited and Clinical Laboratory Improvement Amendments (CLIA) certified laboratory. Genomic alterations, tumor mutational burden (TMB) values, and microsatellite instability (MSI) status were assessed with a mean coverage of 1000X, including single base substitutions, short and long insertion/deletions, copy number variations, gene fusions, and rearrangements. Genomic data and immune checkpoint inhibitors (ICIs) treatment outcome of a cohort of 1610 patients with solid tumors were derived from cBioPortal (MSKCC, Nat Genet. 2019). Results: AKT1/2/3 were found to be mutually exclusive with each other and accounted for 3.4% in this cohort. The frequencies of AKT1/2/3 variations were 1.1%, 1.6%, and 0.8%, respectively. The most common co-altered genes associated with AKT1/2/3 variations were TP53 (69.4%), PIK3CA (19.3%), KRAS (19%), CCNE1 (18.4%), CDKN2A (16.6%), and 11q13 (6.5%). AKT1/2/3 variations were significantly associated with higher TMB, and independent of MSI status. Outcome data from the MSKCC cohort showed that patients with AKT1/2/3 variations had a remarkable clinical benefit to ICIs treatment compared to patients with wild-type AKT1/2/3 in overall survival (OS) (NA vs 18 months, p = 0.009). Furthermore, AKT1/2/3 variations were independent risk factors of OS (HR: 0.55, 95%CI: 0.34-0.87, p = 0.012). Conclusions: The prevalence of AKT1/2/3 somatic alterations across different types of solid tumors in China was 3.4%. AKT1/2/3 variations were associated with an increased TMB and favorable response to ICIs, suggesting that A KT1/2/3 variations may be biomarkers for guiding anti-AKT agents and ICI treatment.
- Published
- 2020
6. Pan-cancer genomic variation characteristics of CDKN2A/CDKN2B/CCND1 in Chinese patients
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Ruobing Ma, Yuandong Wang, Lei Dai, Li Yang, Li Zhuang, Peng Zhao, Yigang Qian, Songfeng Yu, Honglin Guo, Ming Yao, Qiyong Li, and Ming Wang
- Subjects
Cancer Research ,Cyclin D1 ,Variation (linguistics) ,Oncology ,Pan cancer ,business.industry ,CDKN2A ,CDKN2B ,Cancer research ,Medicine ,Cancer development ,Cell cycle ,business - Abstract
e13519Background: Cell cycle regulation plays a vital role in cancer development, and targeting the aberrant pathway using CDK4/6 inhibitors shows reliable efficacy in tumor suppression. Characteri...
- Published
- 2018
7. Regulation of TLR4-induced IL-6 response in bladder cancer cells by opposing actions of MAPK and PI3K signaling
- Author
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Haiyang Xie, Shenyong Yin, Lei Geng, Yan Wang, Lin Zhou, Yigang Qian, Junfang Deng, Xiaowen Feng, and Shusen Zheng
- Subjects
Lipopolysaccharides ,MAPK/ERK pathway ,Cancer Research ,medicine.medical_specialty ,Lipopolysaccharide Receptors ,Biology ,p38 Mitogen-Activated Protein Kinases ,Phosphatidylinositol 3-Kinases ,Cell Line, Tumor ,Internal medicine ,medicine ,Humans ,Extracellular Signal-Regulated MAP Kinases ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Bladder cancer ,Interleukin-6 ,Cancer ,General Medicine ,medicine.disease ,Gene Expression Regulation, Neoplastic ,Toll-Like Receptor 4 ,Endocrinology ,Urinary Bladder Neoplasms ,Oncology ,Tumor progression ,Cancer cell ,Cancer research ,Signal transduction - Abstract
Toll-like receptor 4 (TLR4) was found to be aberrantly expressed in bladder cancer, inducing some genes expression and facilitating tumor progression. Recent data suggest that tumor associated Interleukin-6 (IL-6) correlates with tumor size and grade in bladder cancer. However, the molecule mechanisms of the induction of IL-6 response in bladder cancer cells are not well elucidated. In this study, we manage to find out whether TLR4 signaling is involved in the production of IL-6 by human bladder cancer cells, and the detailed molecule mechanisms by which IL-6 is up-regulated. We selected human bladder cancer T24 cell line in the present study, and examined its expression of TLR4 and CD14 by using flow cytometry. TLR4 signaling was activated by lipopolysaccharide (LPS) and IL-6 secretion in culture supernatants was tested by using ELISA kit. The expression of p38, ERK, JNK and Akt were determined by western-blot analysis using specific antibodies. Our study demonstrated that CD14 and TLR4 were constitutively expressed in T24 cells and activation of TLR4 signaling by LPS resulted in phosphorylation of MAPK and PI3K pathways and up-regulation of IL-6 in dose- and time-dependent manner. Pretreatment of cells with SB203580 (inhibitor of p38) and PD98059 (inhibitor of ERK) attenuated LPS-induced IL-6 expression, whereas LY294002 (inhibitor of PI3K) markedly amplified the LPS-stimulated synthesis of IL-6. Our results demonstrate that activation of TLR4 signaling in bladder cancer cells induces tumor-associated IL-6 expression via activation of p38 and ERK, whereas activation of PI3K/Akt exerts an opposing action.
- Published
- 2008
8. Involvement of p38 mitogen-activated protein kinase pathway in honokiol-induced apoptosis in a human hepatoma cell line (hepG2)
- Author
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Lin Zhou, Yigang Qian, Sheng Yan, Guoping Jiang, Junfang Deng, Haiyang Xie, Lei Geng, Jie Chen, Xiaohui Wang, and Shusen Zheng
- Subjects
MAPK/ERK pathway ,Honokiol ,Hepatology ,biology ,Chemistry ,p38 mitogen-activated protein kinases ,Cytochrome c ,Bcl-xL ,Molecular biology ,chemistry.chemical_compound ,Downregulation and upregulation ,Apoptosis ,biology.protein ,Protein kinase A - Abstract
Background: Honokiol has been known to have antitumour activity. This study was conducted to evaluate the antiproliferative potential of honokiol against the hepG2 heptocellular cell line and its mechanism of action. Methods: hepG2 cells were treated with honokiol of 0–40 μg/ml concentration. The cytotoxic effect of honokiol was determined by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis was evaluated by flow cytometry. Western blots were used to analyse the expression of various proteins (procaspase-9, procaspase-3, cleaved caspase-3, cytochrome c, Bcl-2, Bax, Bad, Bcl-XL and p38). Results: Honokiol induced apoptosis with a decreased expression of procaspase-3 and -9 and an increased expression of active caspase-3. Exposure of hepG2 cells to honokiol resulted in the downregulation of Bcl-XL and Bcl-2 expression and the release of mitochondrial cytochrome c to the cytosol. In addition, honokiol activated the p38 mitogen-activated protein kinase (MAPK) pathway, and the inhibition of this pathway by SB203580 reduced honokiol-induced apoptosis and activation of caspase-3. Conclusion: Honokiol induces apoptosis of hepG2 human hepatocellular carcinoma cells through activation of the p38 MAPK pathway, and, in turn, activation of caspase-3.
- Published
- 2008
9. TLR4 Signaling Induces B7-H1 Expression Through MAPK Pathways in Bladder Cancer Cells
- Author
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Junfang Deng, Junwei Liu, Shenyong Yin, Lin Zhou, Zhou Ye, Yan Wang, Guoping Jiang, Shusen Zheng, Yigang Qian, Lei Geng, Haiyang Xie, and Xiaowen Feng
- Subjects
Lipopolysaccharides ,MAPK/ERK pathway ,Cancer Research ,MAP Kinase Signaling System ,Pyridines ,Morpholines ,Lipopolysaccharide Receptors ,Biology ,B7-H1 Antigen ,Phosphatidylinositol 3-Kinases ,Immune system ,Antigen ,Antigens, CD ,Cell Line, Tumor ,medicine ,Humans ,Phosphorylation ,Extracellular Signal-Regulated MAP Kinases ,Receptor ,Protein Kinase Inhibitors ,Phosphoinositide-3 Kinase Inhibitors ,Anthracenes ,Flavonoids ,Carcinoma, Transitional Cell ,Bladder cancer ,Imidazoles ,JNK Mitogen-Activated Protein Kinases ,General Medicine ,medicine.disease ,Neoplasm Proteins ,Up-Regulation ,Cell biology ,Toll-Like Receptor 4 ,Urinary Bladder Neoplasms ,Oncology ,Chromones ,Cell culture ,TLR4 ,Protein Processing, Post-Translational ,Proto-Oncogene Proteins c-akt - Abstract
TLR4 (Toll-like receptor 4) and B7-H1, which were known to be restricted to immune cells in the past, were found to be aberrantly expressed in a majority of tumor cells, facilitating tumor evasion from immune surveillance. Our study demonstrated that activation of TLR4 signaling in bladder cancer cells up-regulated B7-H1 expression. Furthermore, this regulation was significantly attenuated by ERK or JNK inhibitor. Our results elucidated the molecule mechanism of regulation of B7-H1 expression through TLR4 signaling and may suggest new strategies of down-regulating the cancer-associated B7-H1 expression for bladder cancer treatment.
- Published
- 2008
10. The Role of Toll-Like Receptors 2 and 4 in Acute Allograft Rejection After Liver Transplantation
- Author
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Xiaowen Feng, Shu Zheng, Lei Geng, Yigang Qian, Yu Wang, H.-Y. Xie, Junfang Deng, and Hui Li
- Subjects
Graft Rejection ,Time Factors ,medicine.medical_treatment ,CD14 ,Lipopolysaccharide Receptors ,Antigen-Presenting Cells ,Endogeny ,Liver transplantation ,Monocytes ,Flow cytometry ,Antigens, CD ,Reference Values ,medicine ,Humans ,Receptor ,Transplantation ,Innate immune system ,medicine.diagnostic_test ,business.industry ,Toll-Like Receptor 2 ,Liver Transplantation ,Toll-Like Receptor 4 ,Allograft rejection ,Acute Disease ,Steroid pulse ,Immunology ,Surgery ,business ,Follow-Up Studies - Abstract
Toll-like receptors (TLRs) are germline-encoded receptors expressed on antigen-presenting cells (APCs) that identify a variety of microbial and endogenous ligands and activate the innate immune responses to the presence of danger. However, their role in the development of allograft rejection after liver transplantation remains unknown. In this study, we used flow cytometry to assess TLR-4 and TLR-2 expression among circulating CD14+ monocytes in 64 liver transplant patients and 24 healthy volunteers. We demonstrated significantly higher TLR-2 and TLR-4 expression on circulating monocytes among conditioned liver transplantation recipients with acute rejection compared with those in clinically stable with normal liver function. Steroid pulse therapy significantly reduced the expression of TLR-4 and TLR-2 on the monocytes of recipients with acute rejection. Based on these data, we have suggested that activation of innate immunity in liver transplant recipients through TLR-4 and TLR-2 contributes to the development of acute allograft rejection after liver transplantation. The reduced expression of TLR-4 and TLR-2 may be one of the mechanisms by which steroid pulse therapy inhibits the development of acute rejection. Estimation of TLR expression on APCs may be predictive of in acute rejection after liver transplantation.
- Published
- 2007
11. Involvement of ERK and JNK pathways in IFN-γ-induced B7-DC expression on tumor cells
- Author
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Ming Zhang, Lei Geng, Yan Wang, Shusen Zheng, Junfang Deng, Yigang Qian, Lin Zhou, Guoping Jiang, and Haiyang Xie
- Subjects
MAPK/ERK pathway ,Cancer Research ,Programmed Cell Death 1 Ligand 2 Protein ,MAP Kinase Kinase 4 ,p38 mitogen-activated protein kinases ,Blotting, Western ,Biology ,p38 Mitogen-Activated Protein Kinases ,Interferon-gamma ,Immunity ,Cell Line, Tumor ,Neoplasms ,medicine ,Humans ,Interferon gamma ,RNA, Messenger ,Phosphorylation ,Regulation of gene expression ,Mitogen-Activated Protein Kinase 1 ,Analysis of Variance ,Mitogen-Activated Protein Kinase 3 ,Reverse Transcriptase Polymerase Chain Reaction ,General Medicine ,Janus Kinase 2 ,Flow Cytometry ,Cell biology ,Gene Expression Regulation, Neoplastic ,Oncology ,Cell culture ,B7-1 Antigen ,Signal transduction ,Proto-Oncogene Proteins c-akt ,medicine.drug ,Signal Transduction - Abstract
B7-DC on tumor cells was demonstrated to promote tumor immunity; however, the precise mechanism responsible for the aberrant B7-DC expression remains unknown. Interferon gamma (IFN-γ) can induce B7-DC expression on macrophages and has been shown to regulate anti-tumor immunity by various mechanisms. This study was designed to investigate the relationship of IFN-γ and B7-DC on tumor cells and further explored the signal transduction pathways involved.RT-PCR and flow cytometry were used for the analysis of B7-DC expression on various tumor cells. The phosphorylation of p38, ERK1/2, JNK, Akt, and JAK2 was determined by Western blot.IFN-γ markedly up-regulated B7-DC expression on various tumor cells and resulted in the phosphorylation of JAK2, JNK, ERK, p38, and Akt. Inhibition of ERK or JNK pathway significantly decreased IFN-c-induced B7-DC expression, whereas inhibition of phosphorylation of Akt, p38, and JAK2 had very little effect on IFN-γ-induced B7-DC expression.Our findings demonstrate that the pretreatment of tumor cells with IFN-γ enhances B7-DC expression through ERK and JNK pathways.
- Published
- 2009
12. Involvement of p38 mitogen-activated protein kinase pathway in honokiol-induced apoptosis in a human hepatoma cell line (hepG2)
- Author
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Junfang, Deng, Yigang, Qian, Lei, Geng, Jie, Chen, Xiaohui, Wang, Haiyang, Xie, Sheng, Yan, Guoping, Jiang, Lin, Zhou, and Shusen, Zheng
- Subjects
Carcinoma, Hepatocellular ,Pyridines ,Biphenyl Compounds ,Blotting, Western ,Imidazoles ,Tetrazolium Salts ,Apoptosis ,Flow Cytometry ,p38 Mitogen-Activated Protein Kinases ,Lignans ,Thiazoles ,Caspases ,Cell Line, Tumor ,Humans ,Cell Proliferation ,Signal Transduction - Abstract
Honokiol has been known to have antitumour activity. This study was conducted to evaluate the antiproliferative potential of honokiol against the hepG2 heptocellular cell line and its mechanism of action.hepG2 cells were treated with honokiol of 0-40 microg/ml concentration. The cytotoxic effect of honokiol was determined by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis was evaluated by flow cytometry. Western blots were used to analyse the expression of various proteins (procaspase-9, procaspase-3, cleaved caspase-3, cytochrome c, Bcl-2, Bax, Bad, Bcl-X(L) and p38).Honokiol induced apoptosis with a decreased expression of procaspase-3 and -9 and an increased expression of active caspase-3. Exposure of hepG2 cells to honokiol resulted in the downregulation of Bcl-X(L) and Bcl-2 expression and the release of mitochondrial cytochrome c to the cytosol. In addition, honokiol activated the p38 mitogen-activated protein kinase (MAPK) pathway, and the inhibition of this pathway by SB203580 reduced honokiol-induced apoptosis and activation of caspase-3.Honokiol induces apoptosis of hepG2 human hepatocellular carcinoma cells through activation of the p38 MAPK pathway, and, in turn, activation of caspase-3.
- Published
- 2008
13. B7-H1 up-regulated expression in human pancreatic carcinoma tissue associates with tumor progression
- Author
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Dongsheng Huang, Dong-Lin Li, Junfang Deng, Guoping Jiang, Jian Zhang, Junwei Liu, Zhenhua Hu, Yigang Qian, Shusen Zheng, and Lei Geng
- Subjects
Male ,Cancer Research ,Pathology ,medicine.medical_specialty ,Pancreatic disease ,Cellular differentiation ,Biology ,B7-H1 Antigen ,Antigens, CD ,medicine ,Humans ,RNA, Messenger ,Neoplastic Processes ,Carcinoma ,Cancer ,Cell Differentiation ,General Medicine ,medicine.disease ,Interleukin-10 ,Up-Regulation ,Pancreatic Neoplasms ,medicine.anatomical_structure ,Oncology ,Tumor progression ,Immunohistochemistry ,CA19-9 ,Female ,Pancreas - Abstract
Aberrant tumor cell B7-H1 expression, a member of B7 family that can predominantly stimulate interleukin 10 (IL-10) products, contributed to the tumor immune evasion and tumor progression. This study was designed to investigate the expression of B7-H1 and IL-10 in normal pancreas tissues and pancreatic carcinoma samples, and to evaluate clinical significance of B7-H1 expression in pancreatic carcinoma. First, the B7-H1 and IL-10 expression in 40 pancreatic carcinoma samples and 8 healthy pancreas specimens using reverse transcription-PCR (RT-PCR) and western-blotting was detected. Localization of B7-H1 and IL-10 was confirmed by immunohistochemical (IHC) staining. Next, the association between B7-H1 expression and tumor differentiation and tumor stage was analyzed. Finally, the correlation between tumor-associated B7-H1 and IL-10 was evaluated. Pancreatic carcinoma samples demonstrated the up-regulated expression of B7-H1 and IL-10 at mRNA and protein level compared with normal pancreas tissues. IHC staining revealed that B7-H1 and IL-10 was almost localized in tumor cells. Analysis of relationship between B7-H1 and tumor clinicopathological characteristics showed that B7-H1 expression was significantly associated with poor tumor differentiation (P
- Published
- 2007
14. Regulation of TLR4-induced IL-6 response in bladder cancer cells by opposing actions of MAPK and PI3K signaling.
- Author
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Yigang Qian, Junfang Deng, Haiyang Xie, Lei Geng, Lin Zhou, Yan Wang, Shenyong Yin, Xiaowen Feng, and Shusen Zheng
- Subjects
- *
URINARY organs , *BLADDER cancer , *CANCER invasiveness , *INTERLEUKIN-6 , *CANCER cells - Abstract
Toll-like receptor 4 (TLR4) was found to be aberrantly expressed in bladder cancer, inducing some genes expression and facilitating tumor progression. Recent data suggest that tumor associated Interleukin-6 (IL-6) correlates with tumor size and grade in bladder cancer. However, the molecule mechanisms of the induction of IL-6 response in bladder cancer cells are not well elucidated. In this study, we manage to find out whether TLR4 signaling is involved in the production of IL-6 by human bladder cancer cells, and the detailed molecule mechanisms by which IL-6 is up-regulated. We selected human bladder cancer T24 cell line in the present study, and examined its expression of TLR4 and CD14 by using flow cytometry. TLR4 signaling was activated by lipopolysaccharide (LPS) and IL-6 secretion in culture supernatants was tested by using ELISA kit. The expression of p38, ERK, JNK and Akt were determined by western-blot analysis using specific antibodies. Our study demonstrated that CD14 and TLR4 were constitutively expressed in T24 cells and activation of TLR4 signaling by LPS resulted in phosphorylation of MAPK and PI3K pathways and up-regulation of IL-6 in dose- and time-dependent manner. Pretreatment of cells with SB203580 (inhibitor of p38) and PD98059 (inhibitor of ERK) attenuated LPS-induced IL-6 expression, whereas LY294002 (inhibitor of PI3K) markedly amplified the LPS-stimulated synthesis of IL-6. Our results demonstrate that activation of TLR4 signaling in bladder cancer cells induces tumor-associated IL-6 expression via activation of p38 and ERK, whereas activation of PI3K/Akt exerts an opposing action. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
15. B7-H1 up-regulated expression in human pancreatic carcinoma tissue associates with tumor progression.
- Author
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Lei Geng, Dongsheng Huang, Junwei Liu, Yigang Qian, Junfang Deng, Donglin Li, Zhenhua Hu, Jian Zhang, Guoping Jiang, and Shusen Zheng
- Subjects
TUMORS ,TISSUES ,CANCER cells ,PANCREAS ,CELLS ,MESSENGER RNA ,PATHOLOGY ,CYSTS (Pathology) ,ONCOLOGY - Abstract
Aberrant tumor cell B7-H1 expression, a member of B7 family that can predominantly stimulate interleukin 10 (IL-10) products, contributed to the tumor immune evasion and tumor progression. This study was designed to investigate the expression of B7-H1 and IL-10 in normal pancreas tissues and pancreatic carcinoma samples, and to evaluate clinical significance of B7-H1 expression in pancreatic carcinoma. First, the B7-H1 and IL-10 expression in 40 pancreatic carcinoma samples and 8 healthy pancreas specimens using reverse transcription-PCR (RT-PCR) and western-blotting was detected. Localization of B7-H1 and IL-10 was confirmed by immunohistochemical (IHC) staining. Next, the association between B7-H1 expression and tumor differentiation and tumor stage was analyzed. Finally, the correlation between tumor-associated B7-H1 and IL-10 was evaluated. Pancreatic carcinoma samples demonstrated the up-regulated expression of B7-H1 and IL-10 at mRNA and protein level compared with normal pancreas tissues. IHC staining revealed that B7-H1 and IL-10 was almost localized in tumor cells. Analysis of relationship between B7-H1 and tumor clinicopathological characteristics showed that B7-H1 expression was significantly associated with poor tumor differentiation ( P < 0.01) and advanced tumor stage ( P < 0.01). Meanwhile, tumor-associated B7-H1 expression was also correlated with IL-10 products ( P < 0.01, R
2 = 0.6985, mRNA level; P < 0.01, R2 = 0.7236, protein level) in tumor cells. Our findings for the first time demonstrated up-regulated B7-H1 expression in human pancreatic carcinoma tissues, which might play a role in tumor progression and invasiveness. This expression seemed to be related to the ability of B7-H1 to promoting IL-10 secretion. [ABSTRACT FROM AUTHOR]- Published
- 2008
- Full Text
- View/download PDF
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