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Updated: Jun 26, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

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

Published on: October 27, 2020

Ras alters epithelial-mesenchymal transition in response to TGFbeta by reducing actin fibers and cell-matrix adhesion

Alfiya F Safina1, Andrea E Varga, Anna Bianchi

  • 1Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, New York 14263, USA

Cell Cycle (Georgetown, Tex.)
|January 30, 2009
PubMed

Insights

Transforming growth factor-beta (TGF-beta) induces epithelial-mesenchymal transition (EMT), but activated Ras (RasV12) enhances cell invasion. RasV12 confers metastatic potential by altering TGF-beta

Area of Science:

  • Cell biology
  • Cancer research
  • Molecular oncology

Background:

  • Epithelial-mesenchymal transition (EMT) is crucial for tumor invasion and metastasis.
  • The interplay between TGF-beta and Ras signaling in EMT is not fully understood.

Purpose of the Study:

  • To investigate the distinct and combined roles of TGF-beta and Ras signaling in regulating EMT, cell invasion, and metastatic potential.

Main Methods:

  • Analysis of TGF-beta and RasV12 effects on EMT markers, cell junctions, and actin cytoskeleton.
  • Investigated Smad transcription factor involvement in TGF-beta-induced EMT and RasV12-mediated inhibition.
  • Utilized soft agar assays and animal studies to assess metastatic potential.

Main Results:

  • TGF-beta induces EMT but limits invasion, while RasV12 enhances invasion and counteracts TGF-beta's inhibitory effects.
  • RasV12 inhibits tropomyosin induction and reduces cell-matrix adhesion by preventing Smad4 binding to the TPM1 promoter.
  • RasV12 confers metastatic potential, whereas tropomyosin suppresses tumor growth and metastasis.

Conclusions:

  • TGF-beta-induced EMT alone is insufficient for acquiring invasive potential.
  • Activated Ras signaling significantly alters the TGF-beta response, conferring tumorigenic and invasive capabilities crucial for metastasis.

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