Journal
JOURNAL OF GENETICS AND GENOMICS
Volume 38, Issue 3, Pages 111-116Publisher
SCIENCE CHINA PRESS
DOI: 10.1016/j.jgg.2011.02.001
Keywords
TGF-beta; HSP70; Smad2; EMT
Funding
- National Natural Science Foundation of China [90919058]
- National Basic Research Program of China [2011CB943904, 2011CB943800]
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Smad2 and Smad3, the intracellular mediators of transforming growth factor beta (TGF-beta) signaling, are directly phosphorylated by the activated type I receptor kinase, and then shuttle from the cytoplasm into the nucleus to regulate target gene expression. Here, we report that the 70-kDa heat-shock protein (HSP70) interacts with Smad2 and decreases TGF-beta signal transduction. Ectopic expression of HSP70 prevents receptor-dependent phosphorylation and nuclear translocation of Smad2, and blocks TGF-beta-induced epithelial-mesenchymal transition (EMT) in HaCat cells. Our findings reveal an essential role of HSP70 in TGF-beta-induced epithelial-mesenchymal transition (EMT) by impeding Smad2 phosphorylation.
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