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Updated: Jun 26, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
TGF-beta-induced epithelial to mesenchymal transition
Jian Xu1, Samy Lamouille, Rik Derynck
1Department of Cell and Tissue Biology, Programs in Cell Biology and Developmental Biology, University of California-San Francisco, San Francisco, CA, USA.
Epithelial to mesenchymal transition (EMT) is crucial for development and disease. This review explores how TGF-beta signaling and bone morphogenetic proteins (BMPs) induce EMT, focusing on signaling and transcription mechanisms.
Area of Science:
- Cell Biology
- Developmental Biology
- Cancer Biology
Background:
- Epithelial to mesenchymal transition (EMT) is a fundamental process where cells lose epithelial traits and gain migratory properties.
- EMT is vital during development and implicated in pathological conditions like fibrosis and cancer metastasis.
- TGF-beta signaling is a key inducer of EMT, while bone morphogenetic proteins (BMPs) can also regulate this plasticity.
Purpose of the Study:
- To review the induction of EMT by TGF-beta signaling.
- To focus on the underlying signaling and transcription mechanisms governing EMT.
- To discuss the role of BMPs in regulating epithelial plasticity.
Main Methods:
- Literature review of studies on EMT induction.
- Analysis of signaling pathways involved in EMT.
- Examination of transcriptional regulation during EMT.
Main Results:
- TGF-beta is a potent inducer of EMT in various epithelial cells.
- BMPs can induce either EMT or MET depending on the developmental context.
- Specific signaling and transcription mechanisms mediate TGF-beta-induced EMT.
Conclusions:
- EMT is a critical cellular plasticity mechanism with roles in development and disease.
- Understanding TGF-beta and BMP signaling in EMT is crucial for therapeutic strategies.
- Further research into EMT mechanisms can elucidate its role in tumor progression.
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