MiR-203 Mimic Down-Regulates Baculoviral IAP Repeat Containing 5 Expression and Affects Proliferation and Apoptosis of Gastric Cancer Cells

2020 ◽  
Vol 10 (1) ◽  
pp. 81-86
Author(s):  
Yanhua Xu ◽  
Pailan Peng ◽  
Qiuyuan Zhou
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Real Time Pcr ◽  
Cell Apoptosis ◽  
Bioinformatics Analysis ◽  
Gastric Cancer Cells ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Cancer Bioinformatics

Human baculovirus IAP repeats containing protein 5 (BIRC5) is the most inhibitor of cell apoptosis. Abnormal miR-203 level is associated with the pathogenesis of gastric cancer. Bioinformatics analysis revealed a relationship between miR-203 and BIRC5. Our study assessed miR-203’s role in gastric cancer cells. Tumor tissues and adjacent tissues were collected. miR-203 and BIRC5 mRNA expression in SGC7901 and MKN45 cells was detected by real-time PCR. SGC7901 cells were divided into miR-NC group and miR-203 mimic group followed by analysis of cell proliferation by EdU staining. Compared to adjacent tissues, miR-203 level was decreased and BIRC5 was increased. There was a targeted relationship between miR-203 and BIRC5. Compared with RGM- 1 cells, miR-203 in SGC7901 and MKN45 cells was significantly downregulated and BIRC5 was upregulated. miR-203 mimic significantly downregulated BIRC5 in SGC7901 cells, promoted cell apoptosis, and attenuated cell proliferation. Decreased miR-203 expression and increased BIRC5 expression is associated with the pathogenesis of gastric cancer. MiR-203 can inhibit the expression of BIRC5, inhibit proliferation of gastric cancer cells and induce apoptosis.

scholarly journals LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

scholarly journals miR-504 Promoted Gastric Cancer Cell Proliferation and Inhibited Cell Apoptosis by Targeting RBM4

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yi Zhang ◽  
Hongmei Yong ◽  
Jing Fu ◽  
Guangyi Gao ◽  
Huichang Shi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Normal Group ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Proliferation

Background. The purpose of this study was to explore the role and underlying mechanism of miR-504 and RBM4 in gastric cancer. Methods. The qRT-PCR or Western blot was performed to determine the expressions of miR-504 and RBM4 in the gastric cancer tissues and normal tissues. Human SGC-7901 cells were transfected with miR-504 mimic/inhibitor or pcDNA-RBM4. Cell proliferation and cell apoptosis were assessed by colony formation assay and flow cytometry, respectively. Luciferase reporter gene assays were used to investigate interactions between miR-504 and RBM4 in SGC-7901 cells. Results. The relative expression of miR-504 was significantly upregulated in the gastric cancer group ( n = 25 ) than in the paired normal group ( n = 25 ), but the relative RBM4 expression was remarkably downregulated in the gastric tumor group, compared with the normal group. Additionally, miR-504 overexpression increased the viability of gastric cancer cells. Moreover, RBM4 is a functional target of miR-504 in gastric cancer cells. miR-504 was further confirmed to promote SGC-7901 cell proliferation and inhibit cell apoptosis by downregulation RBM4 in vitro. Conclusions. miR-504 promotes gastric cancer cell proliferation and inhibits cell apoptosis by targeting RBM4, and this provides a potential diagnostic biomarker and treatment for patients with gastric cancer.

scholarly journals Promotion of miR-221-5p on the Sensitivity of Gastric Cancer Cells to Cisplatin and Its Effects on Cell Proliferation and Apoptosis by Regulating DDR1

2020 ◽  
Vol Volume 13 ◽  
pp. 2333-2345
Author(s):  
Xiaomeng Jiang ◽  
Menglin Jiang ◽  
Shuhua Guo ◽  
Pengpeng Cai ◽  
Wei Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Proliferation And Apoptosis

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 CDX2 and Reg IV expression and correlation in gastric cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dandan Chai ◽  
Huifen Du ◽  
Kesheng Li ◽  
Xueliang Zhang ◽  
Xiaoqin Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Real Time ◽  
Real Time Pcr ◽  
Ectopic Expression ◽  
Rank Correlation ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion

Abstract Background Ectopic expression of CDX2 is associated with the development and progression of gastric cancer. Previous studies showed that CDX2 may be an upstream regulator of Reg IV expression in gastric cancer, and our previous report showed that Reg IV upregulated SOX9 expression and enhanced cell migration and invasion in gastric cancer cells. However, the regulatory roles of CDX2 have not been clarified in gastric cancer, and the correlation between CDX2 and Reg IV requires further study. Methods CDX2 and Reg IV were examined in gastric cancer specimens and paired adjacent tissues via real-time PCR and immunohistochemistry (IHC). The association between CDX2 and Reg IV was assessed using the χ2-test and Spearman’s rank correlation. To verify their relationship, knockdown and exogenous expression of CDX2 or Reg IV were performed in AGS and MKN-45 gastric cancer cells, and their expression was subsequently analyzed via a real-time PCR and western blotting. Wound-healing and Transwell assays were used to examine migration and invasion in AGS and MKN-45 cells following CDX2 silencing or overexpression. Results A positive correlation was observed between CDX2 and Reg IV expression at the mRNA and protein levels in gastric cancer tissues. CDX2 silencing significantly downregulated Reg IV expression, and CDX2 overexpression significantly upregulated Reg IV expression in AGS and MKN-45 cells. Neither Reg IV silencing nor overexpression had any effect on CDX2 protein expression in AGS or MKN-45 cells, even though both affected the expression of CDX2 mRNA. Functionally, CDX2 silencing significantly inhibited cell migration and invasion, and CDX2 overexpression significantly promoted cell migration and invasion in AGS and MKN-45 cells. Conclusions Our findings demonstrate that CDX2 expression was positively correlated with that of Reg IV in gastric cancer, and CDX2 promoted cell migration and invasion through upregulation of Reg IV expression in AGS and MKN-45 cells.

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