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Long non-coding RNA CRNDE promotes cell apoptosis by suppressing miR-495 in inflammatory bowel disease

Fan Yang1, Xiao-Fang Li1, Li-Na Cheng1

  • 1Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China.

Experimental Cell Research
|June 29, 2019
PubMed
Abstract

Insights

Long non-coding RNA CRNDE promotes colonic epithelial cell apoptosis in inflammatory bowel diseases (IBD) by suppressing microRNA-495 (miR-495) and increasing SOCS1. CRNDE is a potential therapeutic target for IBD.

Area of Science:

  • Molecular Biology
  • Gastroenterology
  • Immunology

Background:

  • Inflammatory bowel diseases (IBD) involve complex mechanisms of colonic epithelial cell apoptosis.
  • MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) play critical roles in IBD pathogenesis.

Purpose of the Study:

  • To investigate the mechanistic role of lncRNA CRNDE and miR-495 in colonic epithelial cell apoptosis in IBD.
  • To explore the potential of CRNDE as a therapeutic target for IBD.

Main Methods:

  • Dextran sulfate sodium (DSS) induced mouse model of IBD and human colonic epithelial cell lines (HT-29, LOVO, Caco-2) were utilized.
  • RNA interference was employed to down-regulate CRNDE expression.
  • Molecular assays including RNA immunoprecipitation, RNA pull-down, and luciferase reporter assays confirmed molecular interactions.

Main Results:

  • CRNDE and SOCS1 were upregulated, while miR-495 was downregulated in DSS-induced colitis models.
  • CRNDE interference reduced colonic epithelial cell apoptosis and alleviated IBD clinical symptoms in mice.
  • CRNDE was found to promote apoptosis by suppressing miR-495, which targets SOCS1.

Conclusions:

  • CRNDE promotes DSS-induced colonic epithelial cell apoptosis through the miR-495/SOCS1 pathway.
  • CRNDE represents a novel therapeutic target for the treatment of IBD.
Keywords:
ApoptosisInflammatory bowel diseaselncRNA CRNDEp53

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