| Literature DB >> 28986450 |
Yuichi Kitai1, Masashi Iwakami1, Kodai Saitoh1, Sumihito Togi1, Serina Isayama1, Yuichi Sekine1, Ryuta Muromoto1, Jun-Ichi Kashiwakura1, Akihiko Yoshimura2, Kenji Oritani3, Tadashi Matsuda4.
Abstract
Signal-transducing adaptor family member-2 (STAP-2) is an adaptor protein that regulates various intracellular signaling pathways and promotes tumorigenesis in melanoma and breast cancer cells. However, the contribution of STAP-2 to the behavior of other types of cancer cells is unclear. Here, we show that STAP-2 promotes tumorigenesis of prostate cancer cells through up-regulation of EGF receptor (EGFR) signaling. Tumor growth of a prostate cancer cell line, DU145, was strongly decreased by STAP-2 knockdown. EGF-induced gene expression and phosphorylation of AKT, ERK, and STAT3 were significantly decreased in STAP-2-knockdown DU145 cells. Mechanistically, we found that STAP-2 interacted with EGFR and enhanced its stability by inhibiting c-CBL-mediated EGFR ubiquitination. Our results indicate that STAP-2 promotes prostate cancer progression via facilitating EGFR activation.Entities:
Keywords: STAT3; adaptor protein; c-CBL; prostate cancer; protein degradation; signal transduction
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Year: 2017 PMID: 28986450 PMCID: PMC5702677 DOI: 10.1074/jbc.M117.802884
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157