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Updated: Jul 2, 2026

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

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[Can defective TGF-Beta signaling be an Achilles heel in human cancer?]

David A Foster1, Noga Gadir

  • 1Department of Biological Sciences, Hunter College of the City University of New York, New York, NY, USA. foster@genectr.hunter.cuny.edu

AI Zheng = Aizheng = Chinese Journal of Cancer
|August 20, 2008
PubMed

Insights

Cancer cells activate mTOR, blocking cell cycle arrest signals. Rapamycin restores these signals, causing arrest or apoptosis in cancer cells with defective TGF-beta signaling, revealing a therapeutic vulnerability.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Mammalian target of rapamycin (mTOR) is activated by survival signals in cancer cells.
  • mTOR signaling inhibits the transforming growth factor-beta (TGF-beta) pathway, which normally causes cell cycle arrest.
  • Defects in TGF-beta signaling are prevalent in human cancers.

Purpose of the Study:

  • To investigate the role of mTOR and TGF-beta signaling in cancer cell cycle regulation.
  • To explore the therapeutic potential of rapamycin in cancers with defective TGF-beta signaling.

Main Methods:

  • Analysis of mTOR and TGF-beta pathway interactions in cancer cells.
  • Treatment of cancer cells with rapamycin to observe effects on cell cycle progression and apoptosis.

Main Results:

  • Activated mTOR prevents TGF-beta-mediated G1 cell cycle arrest.
  • Rapamycin treatment reactivates TGF-beta signaling, inducing G1 arrest in sensitive cells.
  • Cancer cells with defective TGF-beta signaling undergo apoptosis upon rapamycin treatment, despite not arresting in G1.

Conclusions:

  • Defective TGF-beta signaling represents a potential therapeutic vulnerability in cancer.
  • Rapamycin-based strategies may selectively target cancer cells with compromised TGF-beta pathways.
  • Targeting the interplay between mTOR and TGF-beta signaling offers a rational approach for cancer therapy.

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