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microRNA-141 inhibits TGF-β1-induced epithelial-to-mesenchymal transition through inhibition of the TGF-β1/SMAD2

Sixue Wang1, Mengmeng Zhang1, Tingting Zhang1

  • 1Department of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410000, Hunan, P.R. China.

Archives of Gynecology and Obstetrics
|January 7, 2020
PubMed
Abstract

Insights

MicroRNA-141 (miR-141) inhibits epithelial-to-mesenchymal transition (EMT) and cell proliferation in endometriosis. This study reveals miR-141 as a key regulator of the TGF-β1/SMAD2 pathway, offering new therapeutic targets for endometriosis.

Area of Science:

  • Reproductive biology
  • Molecular oncology
  • Cellular signaling

Background:

  • MicroRNAs (miRNAs) show differential expression in endometriosis.
  • Low expression of miR-141 is observed in endometriosis patients.
  • Epithelial-to-mesenchymal transition (EMT) and TGF-β1/SMAD2 signaling are crucial in tumor progression and invasion.

Purpose of the Study:

  • To investigate the role of miR-141 in regulating the TGF-β1/SMAD2 signaling pathway.
  • To elucidate the association between miR-141 and EMT in endometriosis.
  • To understand the contribution of EMT to endometriosis development.

Main Methods:

  • Immunohistochemistry and western blot analysis for TGF-β1/SMAD2 and EMT markers.
  • Quantitative reverse-transcription polymerase chain reaction for miR-141 expression.
  • Transwell and CCK-8 assays for cellular invasion and proliferation.
  • Plasmid and shRNA transfection for functional miR-141 assays.

Main Results:

  • miR-141, EMT, and TGF-β1/SMAD2 signaling markers were detected in endometriosis tissues.
  • TGF-β1 induced EMT in Ishikawa cells via SMAD2 activation.
  • miR-141 inhibited TGF-β1-induced EMT, proliferation, and invasion in Ishikawa cells.

Conclusions:

  • miR-141 acts as a novel driver of EMT in endometriosis.
  • A link exists between miR-141 and the TGF-β1/SMAD2 signaling pathway in endometriosis.
  • EMT plays a significant role in the pathogenesis of endometriosis.
Keywords:
EMTEndometriosisTGF-β1/SMAD2 signalling pathwaymiR-141

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