期刊
ONCOGENE
卷 35, 期 33, 页码 4388-4398出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.446
关键词
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资金
- MOST [2012CB966600]
- NSFC [31571447, 31090360]
- NIH [R01GM63773, R01 AR053591, R01CA108454, R01DK073932]
- Project 985
- Fundamental Research Funds for Central Universities
- Project 111
Smad and STAT proteins are critical signal transducers and transcription factors in controlling cell growth and tumorigenesis. Here we report that the STAT3 signaling pathway attenuates transforming growth factor-beta (TGF-beta)-induced responses through a direct Smad3-STAT3 interplay. Activated STAT3 blunts TGF-beta-mediated signaling. Depletion of STAT3 promotes TGF-beta-mediated transcriptional and physiological responses, including cell cycle arrest, apoptosis and epithelial-to-mesenchymal transition. STAT3 directly interacts with Smad3 in vivo and in vitro, resulting in attenuation of the Smad3-Smad4 complex formation and suppression of DNA-binding ability of Smad3. The N-terminal region of DNA-binding domain of STAT3 is responsible for the STAT3-Smad3 interaction and also indispensable for STAT3-mediated inhibition of TGF-beta signaling. Thus, our finding illustrates a direct crosstalk between the STAT3 and Smad3 signaling pathways that may contribute to tumor development and inflammation.
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