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MicroRNA-31 Function as a Suppressor Was Regulated by Epigenetic Mechanisms in Gastric Cancer.

Gastric cancer is one of the most lethal malignancies worldwide. The aberrant expression of microRNA-31 (miR-31) has been reported in gastric cancer; however, its regulation mechanisms are still unclear. Here, we confirmed that miR-31 expression was significantly decreased in gastric cancer tissue a...

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Published in:BioMed Research International Vol. 2017; pp. 1 - 12
Main Authors: Wei, Jun, Wang, Zijian, Wang, Zhixiang, Yang, Yong, Fu, Changlai, Zhu, Jianqing, Jiang, Danbin
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell 12/03/2017
Online Access:View this record in EBSCOhost
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      dt: 12/03/2017
      vid: 2017
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        126527107
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        10.1155/2017/5348490
        126527107
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      ppct: 11
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        atl: MicroRNA-31 Function as a Suppressor Was Regulated by Epigenetic Mechanisms in Gastric Cancer.
      aug:
        au:
          Wei, Jun
          Wang, Zijian
          Wang, Zhixiang
          Yang, Yong
          Fu, Changlai
          Zhu, Jianqing
          Jiang, Danbin
        affil: Department of Gastroenterology, Yancheng Affiliated Hospital of Southeast University, Yancheng 224000, China
      sug:
        subj:
          MicroRNA
          Epigenomics
          Stomach Neoplasms
          Human
          Polymerase Chain Reaction
          Gene Expression
      ab: Gastric cancer is one of the most lethal malignancies worldwide. The aberrant expression of microRNA-31 (miR-31) has been reported in gastric cancer; however, its regulation mechanisms are still unclear. Here, we confirmed that miR-31 expression was significantly decreased in gastric cancer tissue and cell lines. Ectopic expression of miR-31 potentially suppresses proliferation and induced early apoptosis in gastric cancer cells. Furthermore, miR-31 expression was regulated as a result of epigenetic mechanisms. The downregulation of miR-31 was associated with promoter DNA methylation status in gastric cancer and cell lines. Moreover, we found that HDAC2 was the direct target of miR-31 by binding to 3′-UTR from the results of luciferase reporter assays, qRT-PCR, and western blotting. HDAC2 played an activation role in tumor growth, whose expression is upregulated and inversely associated with miR-31 levels. All the results suggested that miR-31 function as a crucial tumor suppressor was regulated by epigenetic mechanisms in gastric cancer. We found an epigenetic pathway loop, DNA methylation-miRNA expression-target gene-tumor progression in gastric cancer, and also provided implications for molecular diagnosis and therapeutics of gastric malignancies by detecting miR-31 as a potential target.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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