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Updated: Jul 11, 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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TGF-β, EMT, and resistance to anti-cancer treatment

Xuecong Wang1, Pieter Johan Adam Eichhorn2, Jean Paul Thiery3

  • 1Guangzhou National Laboratory, Guangzhou, China; Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Seminars in Cancer Biology
|November 9, 2023
PubMed

Insights

Transforming growth factor-β (TGF-β) signaling drives epithelial-to-mesenchymal transition (EMT), promoting cancer cell invasion and treatment resistance. Understanding this process is key to developing new cancer therapies.

Area of Science:

  • Cellular biology
  • Molecular oncology
  • Cancer research

Background:

  • Transforming growth factor-β (TGF-β) signaling is crucial for normal development and homeostasis.
  • During cancer progression, TGF-β signaling can be dysregulated, promoting tumor growth and spread.
  • Epithelial-to-mesenchymal transition (EMT) is a developmental process co-opted by cancer cells.

Purpose of the Study:

  • To discuss the role of EMT in carcinoma cell plasticity.
  • To explore the influence of TGF-β on cancer progression and function.
  • To examine the tumor microenvironment and its relation to treatment resistance.

Main Methods:

  • Literature review and synthesis of existing research on TGF-β signaling, EMT, and cancer biology.
  • Analysis of the molecular mechanisms underlying TGF-β-induced EMT.
  • Exploration of the cellular composition of the tumor microenvironment.

Main Results:

  • TGF-β signaling promotes EMT, enhancing carcinoma cell invasion, metastasis, and immune evasion.
  • EMT contributes to chemotherapy resistance by altering cancer cell phenotypes.
  • The tumor microenvironment plays a significant role in mediating these effects.

Conclusions:

  • EMT is a critical mechanism of cancer cell plasticity driven by TGF-β.
  • Dysregulated TGF-β/EMT signaling contributes to aggressive cancer phenotypes and treatment failure.
  • Targeting TGF-β and EMT pathways may offer novel therapeutic strategies for cancer treatment resistance.
Keywords:
Chemotherapy resistanceEMTImmune evasionPartial EMTTGF-β

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