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TGF-beta and epithelial-to-mesenchymal transitions.
Jiri Zavadil1, Erwin P Böttinger
1Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA.
Oncogene
|August 27, 2005
Summary
Epithelial plasticity, crucial for development and disease, is controlled by transforming growth factor-beta (TGF-beta) signaling. Understanding TGF-beta
Area of Science:
- Cell biology
- Molecular biology
- Developmental biology
Background:
- Epithelial cells exhibit remarkable phenotype plasticity, essential for morphogenesis, repair, and tumor invasiveness.
- Epithelial-to-mesenchymal transition (EMT) is an advanced form of epithelial plasticity, critical for understanding various physiological and pathological processes.
Purpose of the Study:
- To review the distinct physiological contexts of epithelial-to-mesenchymal transition (EMT).
- To elucidate the molecular signaling networks controlled by transforming growth factor-beta (TGF-beta) in regulating EMT.
- To highlight the importance of understanding EMT for developing therapeutic strategies.
Main Methods:
- Literature review of studies on epithelial plasticity and EMT.
- Analysis of molecular signaling pathways activated by TGF-beta.
- Integration of signaling networks involving transcriptional regulators.
Main Results:
- Transforming growth factor-beta (TGF-beta) family members initiate and maintain EMT across diverse biological systems.
- TGF-beta activates major signaling pathways and transcriptional regulators, forming complex networks.
- Distinct physiological contexts of EMT are influenced by specific TGF-beta-mediated signaling.
Conclusions:
- A comprehensive understanding of TGF-beta's role in EMT is vital for therapeutic development.
- Targeting TGF-beta signaling pathways offers potential for controlling EMT in disease.
- Further research into the intricate signaling networks governing EMT is warranted.