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

  • Authors:
    • Junquan Jiao
    • Shaobo Zhang
  • View Affiliations / Copyright

    Affiliations: Center for Cancer Diagnosis and Treatment, Shangluo Central Hospital, Shangluo, Shaanxi 72600, P.R. China, Department of General Surgery, Hong Hui Hospital, Xi'an Jiao Tong University, Xi'an, Shaanxi 710049, P.R. China
    Copyright: © Jiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2685-2693
    |
    Published online on: July 23, 2019
       https://doi.org/10.3892/mmr.2019.10515
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Jiao J and Zhang S: Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation. Mol Med Rep 20: 2685-2693, 2019.
APA
Jiao, J., & Zhang, S. (2019). Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation. Molecular Medicine Reports, 20, 2685-2693. https://doi.org/10.3892/mmr.2019.10515
MLA
Jiao, J., Zhang, S."Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation". Molecular Medicine Reports 20.3 (2019): 2685-2693.
Chicago
Jiao, J., Zhang, S."Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation". Molecular Medicine Reports 20, no. 3 (2019): 2685-2693. https://doi.org/10.3892/mmr.2019.10515
Copy and paste a formatted citation
x
Spandidos Publications style
Jiao J and Zhang S: Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation. Mol Med Rep 20: 2685-2693, 2019.
APA
Jiao, J., & Zhang, S. (2019). Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation. Molecular Medicine Reports, 20, 2685-2693. https://doi.org/10.3892/mmr.2019.10515
MLA
Jiao, J., Zhang, S."Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation". Molecular Medicine Reports 20.3 (2019): 2685-2693.
Chicago
Jiao, J., Zhang, S."Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation". Molecular Medicine Reports 20, no. 3 (2019): 2685-2693. https://doi.org/10.3892/mmr.2019.10515
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