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Updated: Oct 12, 2025

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

Published on: October 27, 2020

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Reversing an Oncogenic Epithelial-to-Mesenchymal Transition Program in Breast Cancer Reveals Actionable Immune

Michelle M Williams1, Sabrina A Hafeez1, Jessica L Christenson1

  • 1Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Pharmaceuticals (Basel, Switzerland)
|November 27, 2021
PubMed

Insights

Metastatic triple-negative breast cancer (mTNBC) metastases are immune suppressed, necessitating new immunotherapy strategies beyond checkpoint inhibitors. Targeting epithelial-to-mesenchymal transition (EMT) reveals immune-suppressing mechanisms in mTNBC.

Area of Science:

  • Oncology
  • Immunology
  • Cancer Biology

Background:

  • Checkpoint inhibitors offer immunotherapy for metastatic triple-negative breast cancer (mTNBC).
  • Not all mTNBC patients respond to current immunotherapies.
  • TNBC metastases exhibit greater immune suppression than primary tumors, indicating a need for combination or novel immunotherapy strategies.

Purpose of the Study:

  • To identify immune-suppressive mechanisms in mTNBC.
  • To investigate the role of oncogenic epithelial-to-mesenchymal transition (EMT) in mTNBC immune evasion.
  • To explore potential therapeutic targets for enhancing anti-tumor immunity in mTNBC.

Main Methods:

  • Review of studies manipulating EMT programs in TNBC models.
  • Analysis of differences between mTNBC and epithelial breast cancer subtypes.
  • Examination of tumor cell metabolism, cytokine milieu, and immune modulator secretion.

Main Results:

  • EMT modulation revealed mechanisms by which mTNBC cells suppress innate and adaptive anti-tumor immunity.
  • Identified pathways include tumor cell metabolism and cytokine secretion.
  • mTNBC utilizes additional immune modulators to evade immune responses.

Conclusions:

  • EMT plays a critical role in mTNBC immune suppression.
  • Targeting EMT-associated pathways may enhance immunotherapy efficacy in mTNBC.
  • Several identified pathways are under investigation as therapeutic targets for mTNBC and other advanced cancers.
Keywords:
epithelial-to-mesenchymal transitionimmune suppressionimmunotherapymetastasistriple negative breast cancer

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