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Sorafenib supresses TGF‐β responsiveness by promoting TGF‐β type II receptor degradation.
Author(s) -
Wang ShiWeigh
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.531.14
Subject(s) - sorafenib , transforming growth factor , hepatic stellate cell , cancer research , epithelial–mesenchymal transition , transforming growth factor beta , cell growth , caveolae , receptor , chemistry , tgf beta receptor 2 , microbiology and biotechnology , medicine , pharmacology , signal transduction , biology , tgf alpha , hepatocellular carcinoma , growth factor , cancer , biochemistry , metastasis
Transforming growth factor‐beta (TGF‐β) family are multifunctional and essential in growth and development. The multi‐kinase inhibitor sorafenib is the FDA approved drug for the treatment of many solid tumor. Previous studies have showed that sorafenib inhibit TGF‐β induced epithelial‐mesenchymal transition (EMT) and tissue fibrosis; but the detailed mechanism remains unknown. In this study, we found that sorafenib specific decreases TGF‐β type II receptor in liver epithelial cell through lipid raft/caveolae‐mediated endocytosis but not in hepatic stellate cell. We next find more detail mechanism to prove this different effect between epithelial and stellate cell. The degradation of TGF‐β type II receptor lead to suppression of TGF‐β signaling. Since TGF‐β have been reported that play important roles in several diseases, our study may provide a potential therapy of TGF‐β related disease. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .