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Updated: Jul 11, 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

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Targeting transforming growth factor-beta signaling

Michael Pennison1, Boris Pasche

  • 1Cancer Genetics Program, Division of Hematology/Oncology, Department of Medicine and Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

Current Opinion in Oncology
|October 2, 2007
PubMed
Abstract

Insights

Excessive transforming growth factor-beta (TGF-β) drives cancer and fibrosis. Targeting TGF-β signaling through various strategies shows promise for treating these conditions.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Transforming growth factor-beta (TGF-β) overproduction by tumors promotes cancer growth and metastasis.
  • TGF-β signaling also contributes to fibrosis by increasing extracellular matrix production.
  • Aberrant TGF-β signaling is implicated in tumor progression and fibrotic disorders.

Purpose of the Study:

  • To review recent advances in strategies for inhibiting TGF-β signaling.
  • To evaluate the potential of these strategies in treating cancer and fibrosis.

Main Methods:

  • Focus on four key strategies to disrupt TGF-β signaling.
  • Discuss techniques for inhibiting TGF-β ligands, receptor kinase activity, and SMAD signaling.
  • Review methods for restoring antitumor immunity via TGF-β inhibition.

Main Results:

  • Inhibition of TGF-β ligands, receptor kinase, and SMAD signaling are primary approaches.
  • Restoring antitumor immunity by inhibiting TGF-β is also a key strategy.
  • Various techniques are employed to implement these four main strategies.

Conclusions:

  • Altered TGF-β signaling is a significant factor in tumor progression, metastasis, and fibrosis.
  • Antagonizing aberrant TGF-β signaling represents a promising therapeutic avenue.
  • Preclinical and clinical data support TGF-β pathway inhibition for cancer and fibrotic diseases.

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