Mo1660 FOXP3 Inhibits Cell Proliferation of Gastric Cancer Cells Through Modulation of the TGF-β/SMAD Signaling Pathway

2014 ◽  
Vol 146 (5) ◽  
pp. S-629
Author(s):  
Liu Yimei ◽  
Ma Guifen ◽  
Shiyao Chen
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Smad Signaling ◽  
Smad Signaling Pathway

scholarly journals Bleomycin Suppresses the Proliferation and the Mobility of Human Gastric Cancer Cells Through the Smad Signaling Pathway

2016 ◽  
Vol 40 (6) ◽  
pp. 1401-1409 ◽  
Author(s):  
Jin-fang Liu ◽  
Xiao-cui Nie ◽  
You-cheng Shao ◽  
Wen-hui Su ◽  
Hai-ying Ma ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Annexin V ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Smad Signaling ◽  
Smad Signaling Pathway

Background/Aims: Extensive studies have demonstrated that Bleomycin (BLM) is a glycopeptide antibiotic that has been used as an anticancer chemotherapeutic reagent. It can induce both single- and double-strand DNA damage, inhibit synthesis of DNA, suppress proliferation, and induce apoptosis in cancer cells. Smad signaling transducers are considered as important molecules in tumor development and progression, and may closely be related to the biological behaviors of some malignant carcinomas, including gastric cancer. Methods: The effects of different concentrations of BLM on the proliferation, cell cycle, apoptosis, migration, and invasion on gastric cancer cell lines MKN45 and AGS were assayed by using CCK-8 assay, Annexin V/PI double staining, PI staining, and transwell assay. Western blot and Immunohistochemistry were applied to analyze the potential mechanism(s). Results: BLM treatment resulted in a low proliferation, high apoptosis, low migration and invasion in MKN45 and AGS cells. Furthermore, the possible mechanisms underlying that Smad3 activity could be changed after binding with BLM, and subsequently the Smad signaling pathway had a cascade response. Conclusion: These results highlight BLM as an exciting theme for gastric cancer treatment, which may represent an effective clinical therapeutic reagent for gastric cancer patients.

scholarly journals MiR-496 Inhibits the Proliferation Through Targeting LYN and AKT/mTOR Signaling Pathway in Gastric Cancer

2020 ◽  
Author(s):  
Rui Su ◽  
Enhong Zhao ◽  
Jun Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Mtor Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Ags Cells

Abstract MiRNA operates as a tumor suppressor or carcinogen to regulate cell proliferation, metastasis, invasion, differentiation, apoptosis and metabolic process. In the present research, we investigated the effect and mechanism of miR496 in human gastric cancer cells. Cell proliferation was measured by CCK8 and clonogenic assay. Transwell test was performed to detect cell migration and invasion. Flow cytometry analysis was used to evaluate cell apoptosis. Bioinformatics software targetscan was used for the screening of miR-496’s target gene. MiR-496 was down regulated in three gastric cancer cell lines, SGC-790, AGS and MKN45 compared with normal gastric epithelial cell line GES-1. MiR-496 mimics inhibited the proliferation of AGS cells after the transfection for 48 h and 72 h. The migration and invasion of AGS cells were also inhibited by the transfection of miR-496 mimics. In addition, miR-496 mimics induced the apoptosis through up regulating the levels of Bax and Active Caspase3 and down regulating the levels of Bcl-2 and Total Caspase3. Bioinformatics analysis showed that there was a binding site between miR-496 and LYN kinase (LYN). MiR-496 mimics could inhibit the expression of LYN in AGS cells. The overexpression of LYN blocked the inhibition of tumor cell growth, as well as the inhibition of AKT/mTOR signaling pathway induced by miR-496 in gastric cancer cells. In conclusion, miR-496 inhibited the proliferation through the AKT/mTOR signaling pathway via targeting LYN in gastric cancer cells. Our research provides a new potential target for clinical diagnosis and targeted treatment of gastric cancer.

miRNA-206 Regulates EVI1 Gene Expression, Akt Signaling Pathway and Cell Biological Behavior in Gastric Cancer Cells

2019 ◽  
Vol 9 (10) ◽  
pp. 1381-1387
Author(s):  
Wanjun Jia ◽  
Yabin Zhang ◽  
Ruian Wang
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Proliferation ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

To investigate the impact of miRNA-206 on the transcriptional expression of EVI1 gene and activation of Akt/JNK signaling pathway in gastric cancer cells, and to provide a new idea for gene-targeted therapy of gastric cancer. The miRNA-206 transfection experiment was firstly used to verify the regulation of EVI1. The experiment was divided into three groups: miRNA-206 mimics (100 nM), miRNA-206 inhibitor (100 nM), miR-NC (100 nM), and transfected into gastric cancer cells sgc7901, Western blot. EVI1 protein expression was detected; then the signal transduction and biological behavior of the cells were verified by miRNA-206 lentiviral vector transfection experiments. The experiment was divided into three groups: pLB-miRNA-206 group, empty vector group and control group (sgc7901 cell group). miRNA-206 and EVI1 mRNA levels were detected by real-time fluorescence quantitative (RT-PCR), and p-Akt and p-JNK were detected by Western blot. Protein expression, cell proliferation was quantified by MTT assay, and the alteration of cell cycle were detected by flow cytometry. miRNA-206 may affect the cell proliferation and division cycle by targeting the regulation of EVI1 transcriptional gene expression and activation of Akt/JNK signaling pathway in gastric cancer cells, and it is expected to provide an important selection site for gene-targeted therapy of gastric cancer.

scholarly journals Knockdown of NCOA2 Inhibits the Growth and Progression of Gastric Cancer by Affecting the Wnt Signaling Pathway–Related Protein Expression

2020 ◽  
Vol 19 ◽  
pp. 153303382092807
Author(s):  
Zhenlv Lin ◽  
Fan Yang ◽  
Dong Lu ◽  
Wenjie Sun ◽  
Guangwei Zhu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Nuclear Receptor ◽  
Wnt Signaling Pathway ◽  
Related Protein ◽  
Gastric Cancer Cells ◽  
Nuclear Receptor Coactivator ◽  
Proliferation And Invasion

Objective: The aim of the study is to determine the role of nuclear receptor coactivator 2 in cell proliferation and invasion ability of gastric cancer cells and to explore its possible mechanisms. Methods: Immunohistochemical staining was used to determine NCOA2 gene expression in gastric cancer. Western blotting was used to detect Wnt signal pathways–related protein expression. Colony formation assays, Cell Counting Kit-8 assays, and transwell assays were used to determine cell proliferation, metastasis, and invasion ability of gastric cancer cells. A flow cytometric apoptosis tests determine gastric cancer cell apoptosis ability after inhibition of the expression of nuclear receptor coactivator 2. Subcutaneous mouse models were used to determine the gastric cancer growth and peritoneal metastasis differences after inhibition the expression of nuclear receptor coactivator 2. Results: The expression of nuclear receptor coactivator 2 in gastric cancer cells is high ( P < .01), including lymph node metastasis, TNM staging, and gender differences in nuclear receptor coactivator 2 expression were statistically significant ( P < .01). Short interfering nuclear receptor coactivator 2 could inhibit the proliferation and invasion ability of gastric cancer cells. Short interfering nuclear receptor coactivator 2 promotes the apoptosis of gastric cancer cells. Animal experiments showed that short interfering nuclear receptor coactivator 2 could inhibit the growth and invasion of gastric cancer-transplantable tumors. Knockdown of the expression of nuclear receptor coactivator 2 inhibited the Wnt/β-catenin signaling pathway in the gastric cancer cells. Conclusions: Knockdown of the expression of nuclear receptor coactivator 2 can inhibit the proliferation and invasion of human gastric cancer in vitro and in vivo. The underlying mechanism of NOCA2 affects the Wnt signaling pathway.

scholarly journals Downregulation of MicroRNA-147 Inhibits Cell Proliferation and Increases the Chemosensitivity of Gastric Cancer Cells to 5-Fluorouracil by Directly Targeting PTEN

2018 ◽  
Vol 26 (6) ◽  
pp. 901-911 ◽  
Author(s):  
Jianjun Shen ◽  
Weina Niu ◽  
Hongbo Zhang ◽  
Ma Jun ◽  
Hongyan Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Expression Patterns ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Apoptosis Pathway

Gastric cancer is the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. This study aimed to investigate the expression patterns, biological roles, and underlying mechanisms of microRNA-147 (miR-147) in gastric cancer. The present study demonstrated that miR-147 was significantly upregulated in gastric cancer tissues and cell lines. Downregulation of miR-147 decreased cell proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-fluorouracil (5-FU) through the cell apoptosis pathway. In addition, phosphatase and tensin homolog (PTEN) was mechanically identified as the direct target of miR-147 in gastric cancer. PTEN knockdown reversed the effects of miR-147 downregulation on the proliferation, chemosensitivity, and 5-FU-induced apoptosis of gastric cancer cells. Moreover, miR-147 regulated the PI3K/AKT signaling pathway in gastric cancer by targeting PTEN. In conclusion, miR-147 suppressed the proliferation and enhanced the chemosensitivity of gastric cancer cells to 5-FU by promoting cell apoptosis through directly targeting PTEN and regulating the PI3K/AKT signaling pathway. This study provides important insight into the molecular mechanism that underlies the chemoresistance of gastric cancer cells. The results of this study could aid the development of a novel therapeutic strategy for gastric cancer.

scholarly journals XEDAR inhibits the proliferation and induces apoptosis of gastric cancer cells by regulating JNK signaling pathway

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Lihong Yang ◽  
Xiaojun Huang ◽  
Wei Wang ◽  
Tao Jiang ◽  
Feifei Ding
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Gastric Cancer Cells ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis ◽  
Cancer Tissues

Abstract X-linked ectodermal dysplasia receptor (XEDAR) has been widely studied in epidermal morphogenesis, but few studies have been conducted on tumorigenesis and development, including gastric cancer. In the present research, we aimed to investigate the effect of XEDAR on gastric cancer and further explore the molecular mechanisms involved. The differential expression of XEDAR in 90 tissue specimens (30 gastric cancer tissues, 30 adjacent tissues and 30 normal tissues) was detected by real-time PCR (RT-PCR) and Western blot. Cell proliferation and apoptosis were explored using MTT and Annexin-V/propidium iodide (PI) assays, respectively. The results revealed that the expression of XEDAR was decreased in gastric cancer tissues and in gastric cancer cell lines, and its expression is regulated by p53 in BGC-823 cells. Furthermore, overexpression of XEDAR inhibited cell proliferation and induced apoptosis in BGC-823 cells. XEDAR moreover inhibited proliferation and induced apoptosis in gastric cancer cells by regulating the JNK signaling pathway. Collectively, the results of the present study suggested that XEDAR inhibits cell proliferation and induces apoptosis by participating in p53-mediated signaling pathway and inhibiting the downstream JNK signaling pathway in gastric cancer.

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