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Updated: Mar 18, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

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miRNA-Mediated KHSRP Silencing Rewires Distinct Post-transcriptional Programs during TGF-β-Induced

Margherita Puppo1, Gabriele Bucci2, Martina Rossi1

  • 1Gene Expression Regulation Laboratory, IRCCS AOU San Martino-IST, 16132 Genova, Italy; DIMES Sezione Biochimica-Università di Genova, 16132 Genova, Italy.

Cell Reports
|July 12, 2016
PubMed

Insights

MicroRNA-27b-3p silences KHSRP, a protein crucial for transforming growth factor beta (TGF-β)-induced epithelial-to-mesenchymal transition (EMT) in mammary cells. This pathway regulates gene expression changes contributing to EMT.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Epithelial-to-mesenchymal transition (EMT) is essential for cancer progression.
  • Transforming growth factor beta (TGF-β) is a key inducer of EMT.

Purpose of the Study:

  • To investigate the role of KHSRP in TGF-β-induced EMT.
  • To elucidate the molecular mechanisms by which KHSRP regulates EMT.

Main Methods:

  • RNA sequencing
  • Gene expression analysis
  • Western blotting
  • RNA immunoprecipitation

Main Results:

  • miR-27b-3p-mediated silencing of KHSRP is required for TGF-β-induced EMT.
  • KHSRP regulates the levels of miR-192-5p and alternative splicing of EMT-related genes.
  • KHSRP cooperates with hnRNPA1 in regulating pre-mRNA splicing.

Conclusions:

  • TGF-β-induced KHSRP silencing is a central event in a pathway that promotes EMT.
  • KHSRP acts as a regulator of gene expression changes associated with EMT.

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