Title: | STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization |
Authors: | Kitai, Yuichi Browse this author →KAKEN DB |
Iwakami, Masashi Browse this author |
Saitoh, Kodai Browse this author |
Togi, Sumihito Browse this author |
Isayama, Serina Browse this author |
Sekine, Yuichi Browse this author |
Muromoto, Ryuta Browse this author →KAKEN DB |
Kashiwakura, Jun-ichi Browse this author |
Yoshimura, Akihiko Browse this author |
Oritani, Kenji Browse this author |
Matsuda, Tadashi Browse this author →KAKEN DB |
Keywords: | adaptor protein |
prostate cancer |
protein degradation |
signal transduction |
STAT3 |
c-CBL |
Issue Date: | 24-Nov-2017 |
Publisher: | American Society for Biochemistry and Molecular Biology (ASBMB) |
Journal Title: | Journal of Biological Chemistry (JBC) |
Volume: | 292 |
Issue: | 47 |
Start Page: | 19392 |
End Page: | 19399 |
Publisher DOI: | 10.1074/jbc.M117.802884 |
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. |
Rights: | This research was originally published in J. Biol. Chem. Kitai,Yuichi et al. STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization. J. Biol. Chem. 2017; 292(47):19392-19399. © the American Society for Biochemistry and Molecular Biology. |
Type: | article |
URI: | http://hdl.handle.net/2115/72029 |
Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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