Journal
ONCOGENE
Volume 24, Issue 37, Pages 5764-5774Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1208927
Keywords
Smad; metastasis; fibrosis; cancer; signal transduction; mesenchyme
Funding
- NIDDK NIH HHS [R01 DK056077, P50 DK064236-010003, R01 DK060043] Funding Source: Medline
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Remarkable phenotype plasticity of epithelial cells underlies morphogenesis, epithelial repair and tumor invasiveness. Detailed understanding of the contextual cues and molecular mediators that control epithelial plasticity will be required in order to develop viable therapeutic approaches targeting epithelial-to-mesenchymal transition (EMT), an advanced manifestation of epithelial plasticity. Members of the transforming growth factor (TGF-beta) family of growth factors can initiate and maintain EMT in a variety of biological systems and pathophysiological context by activating major signaling pathways and transcriptional regulators integrated in extensive signaling networks. Here we will review the distinct physiological contexts of EMT and the underlying molecular signaling networks controlled by TGF-beta.
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