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Long non?coding RNA MEG?3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation.

ABSTRACT: Gastric carcinoma is one of the most frequently diagnosed gastrointestinal tumors. Long non?coding RNAs (lncRNAs) are broadly defined as endogenous cellular non?coding RNA molecules. Studies have demonstrated that they may be associated with human cancer progression. In the present study, the role of lncRNA?maternally expressed gene 3 (MEG3) in the progression of gastric carcinoma cells was investigated in vitro and in vivo. It was demonstrated that lncRNA?MEG3 expression was downregulated in gastric carcinoma cells compared with normal gastric cells. lncRNA?MEG3 transfection increased E?cadherin expression and markedly inhibited gastric carcinoma cell growth, migration and invasion. Flow cytometric analysis revealed that lncRNA?MEG3 transfection promoted the apoptosis of gastric carcinoma cells. Western blot analysis demonstrated that lncRNA?MEG3 transfection inhibited the expression of anti?apoptotic proteins B cell lymphoma-2 (Bcl?2) and Bcl?2?like protein 2 and increased the expression of pro?-apoptotic proteins caspase?3 and caspase?9 in gastric carcinoma cells. lncRNA?MEG3 transfection upregulated the expression of epithelial marker E?cadherin and inhibited the expression of mesenchymal markers vimentin and fibronectin in gastric carcinoma cells, which suggested that lncRNA?MEG3 inhibited epithelial?mesenchymal transition (EMT), which may subsequently inhibit progression in gastric carcinoma cells. The present study also revealed that lncRNA?MEG3 transfection suppressed tumor growth mainly by decreasing the expression of vascular endothelial growth factor and increasing the expression of Bcl?2 in vivo. In conclusion, these results indicated that lncRNA?MEG3 may regulate EMT?associated signaling pathways and has the potential as a therapeutic target in gastric carcinoma.

SUBMITTER: Jiao J

PROVIDER: S-EPMC6691256 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation.

Jiao Junquan J Zhang Shaobo S

Molecular medicine reports 20190723 3

Gastric carcinoma is one of the most frequently diagnosed gastrointestinal tumors. Long non‑coding RNAs (lncRNAs) are broadly defined as endogenous cellular non‑coding RNA molecules. Studies have demonstrated that they may be associated with human cancer progression. In the present study, the role of lncRNA‑maternally expressed gene 3 (MEG3) in the progression of gastric carcinoma cells was investigated in vitro and in vivo. It was demonstrated that lncRNA‑MEG3 expression was downregulated in ga ...[more]

PMID: 31524253

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Project description:BackgroundThe previous investigations have identified that long non-coding RNA (lncRNAs) act as crucial regulators in gastric carcinoma. However, the function of lncRNA MIR4435-2HG in the modulation of gastric carcinoma remains elusive. Here, we aimed to explore the role of MIR4435-2HG in gastric carcinoma.MethodThe Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were applied to select the differently expressed lncRNAs in gastric carcinoma. The qRT-PCR was applied to analyze MIR4435-2HG expression in carcinoma tissues and cell lines. The effect of MIR4435-2HG on proliferation, invasion, migration, and apoptosis of gastric carcinoma cells was detected by Cell Counting Kit-8 (CCK-8) assays, transwell assays, and flow cytometry in vitro. A subcutaneous tumor model was constructed to examine the tumor growth of gastric carcinoma cells after knocking out MIR4435-2HG. RNA immunoprecipitation and luciferase reporting assays were applied to evaluate the interaction of MIR4435-2HG, miR-138-5p, and Sox4.ResultsThe bioinformatics analysis based on TCGA and GEO databases indicated that MIR4435-2HG was obviously elevated in gastric carcinoma samples. The qRT-PCR analysis revealed that MIR4435-2HG was upregulated in clinical gastric carcinoma tissues and cells. The high expression of MIR4435-2HG is associated with the poor survival rate of patients. The knockout of MIR4435-2HG could repress the proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) and accelerate the apoptosis of gastric carcinoma cells. Moreover, the deletion of MIR4435-2HG was able to attenuate the tumor growth in vivo. Mechanically, we identified that MIR4435-2HG enhanced Sox4 expression by directly interacting with miR-138-5p as a competitive endogenous RNA (ceRNA) in gastric carcinoma cells, in which Sox4 was targeted by miR-138-5p.ConclusionMIR4435-2HG is elevated in gastric carcinoma cells and contributes to the growth, metastasis, and EMT of gastric carcinoma cells by targeting miR-138-5p/Sox4 axis. MIR4435-2HG may be applied as a potential therapeutic target in gastric carcinoma.

Dataset Information

Long non?coding RNA MEG?3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation.

Publications

Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation.

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