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The Drosha-Independent MicroRNA6778-5p/GSK3β Axis Mediates the Proliferation of Gastric Cancer Cells

Mingjun Ren1,2, Li Xing3, Wanping Wang3

  • 1Department of Laboratory Medicine, Liuzhou People's Hospital, Liu Zhou 545006, China.

Computational Intelligence and Neuroscience
|October 10, 2022
PubMed
Abstract

Insights

MicroRNA6778-5p (miR6778-5p) promotes gastric cancer cell proliferation when Drosha expression is low. This occurs by targeting glycogen synthase kinase-3β (GSK3β), offering potential therapeutic insights for gastric cancer.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • Gastric cancer (GC) remains a leading cause of cancer mortality worldwide.
  • Drosha is implicated in tumor development, with its downregulation observed in some GC cells.
  • An inverse correlation between Drosha and microRNA6778-5p (miR6778-5p) expression was unexpectedly noted in GC.

Purpose of the Study:

  • To investigate the role of miR6778-5p in the proliferation of gastric cancer cells with reduced Drosha expression.
  • To elucidate the underlying molecular mechanism by which miR6778-5p influences gastric cancer cell growth.

Main Methods:

  • Construction of Drosha knockdown lentivirus and transfection into gastric cancer cells.
  • Manipulation of miR6778-5p levels using mimics and inhibitors in Drosha-deficient cells.
  • Assessment of cell proliferation via Cell Counting Kit-8 (CCK-8) assays.
  • Bioinformatic prediction and experimental validation of miR6778-5p targeting of glycogen synthase kinase-3β (GSK3β).

Main Results:

  • Drosha knockdown significantly reduced Drosha mRNA and protein levels in gastric cancer cells.
  • Overexpression of miR6778-5p enhanced proliferation in Drosha low-expressing cells, while knockdown inhibited it.
  • miR6778-5p was predicted and validated to target GSK3β, leading to decreased GSK3β mRNA and protein levels upon miR6778-5p overexpression.

Conclusions:

  • miR6778-5p promotes the proliferation of gastric cancer cells with low Drosha expression.
  • The mechanism involves targeting and downregulating glycogen synthase kinase-3β (GSK3β).

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