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Updated: May 21, 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

Regulation of EMT by TGFβ in cancer

Carl-Henrik Heldin1, Michael Vanlandewijck, Aristidis Moustakas

  • 1Ludwig Institute for Cancer Research, Uppsala University, Box 595, SE-751 24 Uppsala, Sweden. c-h.heldin@licr.uu.se

FEBS Letters
|June 20, 2012
PubMed

Insights

Transforming growth factor-β (TGFβ) initially suppresses tumors but promotes advanced cancer by inducing epithelial-mesenchymal transition (EMT), enhancing metastasis and altering the tumor microenvironment. Targeting EMT offers new cancer therapy strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Transforming growth factor-β (TGFβ) plays a dual role in cancer, initially suppressing tumors by inhibiting cell growth and promoting apoptosis.
  • In advanced cancers, TGFβ paradoxically promotes tumor progression by inducing epithelial-mesenchymal transition (EMT), increasing invasiveness and metastasis.
  • TGFβ also impacts the tumor microenvironment by suppressing immune surveillance and promoting angiogenesis.

Purpose of the Study:

  • To elucidate the mechanisms by which TGFβ promotes tumor progression in advanced cancers.
  • To highlight the role of TGFβ-induced epithelial-mesenchymal transition (EMT) in cancer invasiveness and metastasis.
  • To identify TGFβ and EMT pathways as potential targets for cancer diagnosis, prognosis, and therapy.

Main Methods:

  • The study reviews existing literature on TGFβ signaling pathways and their impact on cancer progression.
  • Analysis focuses on the transcriptional and posttranscriptional regulation of transcription factors involved in EMT.
  • Comparison of EMT pathways with stem cell programs is discussed.

Main Results:

  • TGFβ induces EMT by regulating transcription factors that suppress epithelial characteristics and enhance mesenchymal features.
  • EMT involves changes in cell junctions, polarity, matrix production, and secretion of migration-stimulating factors.
  • The EMT program shares similarities with stem cell programs, suggesting a link to cancer stem cells.

Conclusions:

  • TGFβ's pro-tumorigenic effects in advanced cancers are mediated by EMT, contributing to invasiveness and metastasis.
  • TGFβ also influences the tumor microenvironment, supporting tumor growth and spread.
  • Targeting inducers and effectors of EMT presents a promising avenue for developing novel cancer diagnostics, prognostics, and therapeutics.

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