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MiR-22 suppresses epithelial-mesenchymal transition in bladder cancer by inhibiting Snail and MAPK1/Slug/vimentin

Mingjie Xu1, Jiangfeng Li1, Xiao Wang1

  • 1Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Cell Death & Disease
|February 14, 2018
PubMed

Insights

MicroRNA-22 (miR-22) is downregulated in bladder cancer (BCa). Restoring miR-22 inhibits BCa cell proliferation, migration, and invasion by targeting MAPK1 and Snail, suppressing EMT.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) are key regulators in cancer development.
  • The role of miR-22 in bladder cancer (BCa) is not fully understood.
  • Previous studies show miR-22 acting as both a tumor suppressor and oncomiR in different cancers.

Purpose of the Study:

  • To investigate the expression, function, and mechanism of miR-22 in bladder cancer.
  • To determine miR-22's targets and its role in BCa cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT).

Main Methods:

  • Analysis of miR-22 expression in BCa tissues versus adjacent non-cancerous tissues.
  • In vitro and in vivo experiments to assess the effects of miR-22 overexpression on BCa cells.
  • Target validation using luciferase assays and Western blotting.
  • Statistical analysis of patient data to correlate MAPK1 and Snail expression with prognosis.

Main Results:

  • MiR-22 is significantly downregulated in BCa tissues.
  • Overexpression of miR-22 inhibits BCa cell proliferation, migration, and invasion.
  • MiR-22 directly targets MAPK1 (ERK2) and Snail, suppressing proliferation, apoptosis, and cell motility.
  • Low expression of MAPK1 or Snail is associated with better patient survival.
  • MiR-22 disrupts a positive feedback loop involving MAPK1, Slug, and vimentin, thereby inhibiting EMT.

Conclusions:

  • MiR-22 functions as a tumor suppressor in bladder cancer.
  • MiR-22 inhibits BCa progression by targeting MAPK1 and Snail and disrupting the MAPK1/Slug/vimentin feedback loop.
  • Targeting this miR-22-mediated pathway offers a potential therapeutic strategy for BCa treatment.

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