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Updated: Aug 27, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
TGF-β in developmental and fibrogenic EMTs
1Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Transforming growth factor-beta (TGF-β) and RAS-MAPK signaling pathways cooperate to induce epithelial-mesenchymal transitions (EMTs). This interaction is crucial for development, wound healing, fibrosis, and cancer metastasis.
Area of Science:
- Cell Biology
- Molecular Biology
- Developmental Biology
Background:
- Transforming growth factor-beta (TGF-β) is a key inducer of epithelial-mesenchymal transitions (EMTs).
- EMTs are complex processes involving cell proliferation, differentiation, communication, and extracellular matrix remodeling.
- RAS-MAPK signaling is often essential for TGF-β-induced EMTs.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying the cooperation between TGF-β-SMAD and RAS-MAPK pathways in EMT induction.
- To establish mechanistic links between EMT, progenitor cell differentiation, and cancer metastasis.
Main Methods:
- Investigated the interplay between TGF-β-SMAD and RAS-MAPK signaling pathways.
- Analyzed EMT induction in embryonic, adult, and carcinoma epithelial cells.
- Examined the role of EMT in gastrulation and intra-tumoral fibrosis.
Main Results:
- Detailed the molecular basis for TGF-β and RAS-MAPK pathway cooperation in EMT.
- Demonstrated direct mechanistic links between EMT and progenitor cell differentiation during gastrulation.
- Showcased the role of EMT in intra-tumoral fibrosis during cancer metastasis.
Conclusions:
- TGF-β driven EMTs are integral to broader developmental, fibrotic, and metastatic processes.
- Understanding the crosstalk between TGF-β-SMAD and RAS-MAPK pathways provides insights into development and disease.
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