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TGF-β mediated drug resistance in solid cancer

Marta Turati1, Alexandra Mousset2, Nervana Issa2

  • 1Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.

Cytokine & Growth Factor Reviews
|April 26, 2023
PubMed

Insights

Transforming growth factor beta (TGF-β) signaling promotes cancer progression and drug resistance. Targeting TGF-β pathways offers strategies to overcome therapeutic resistance and improve cancer treatment outcomes.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • Transforming growth factor beta (TGF-β) is a crucial signaling molecule with three mammalian isoforms (TGF-β1, -β2, -β3).
  • TGF-β signaling pathways are categorized into SMAD-dependent (canonical) and SMAD-independent (non-canonical) routes, tightly regulated by various mechanisms.
  • TGF-β exhibits a dual role in cancer progression, inhibiting early-stage proliferation while promoting invasion in advanced tumors.

Purpose of the Study:

  • To review mechanisms of TGF-β-mediated drug resistance in cancer.
  • To present current strategies for targeting the TGF-β pathway to enhance therapeutic sensitivity.

Main Methods:

  • Literature review of studies on TGF-β signaling in cancer.
  • Analysis of mechanisms underlying TGF-β-induced drug resistance.
  • Compilation of therapeutic strategies targeting the TGF-β pathway.

Main Results:

  • TGF-β signaling is significantly activated in cancers post-chemotherapy and radiotherapy, contributing to drug resistance.
  • High TGF-β levels are observed in both tumor and stromal cells in advanced cancers.
  • Multiple mechanisms link TGF-β signaling to the development of resistance to cancer therapies.

Conclusions:

  • Understanding TGF-β-mediated drug resistance is critical for improving cancer treatment.
  • Targeting TGF-β signaling pathways presents a promising approach to overcome therapeutic resistance and enhance tumor sensitivity to treatments.
Keywords:
CancerDrug resistanceTransforming growth factor β

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