TY - JOUR
T1 - STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization
AU - Kitai, Yuichi
AU - Iwakami, Masashi
AU - Saitoh, Kodai
AU - Togi, Sumihito
AU - Isayama, Serina
AU - Sekine, Yuichi
AU - Muromoto, Ryuta
AU - Kashiwakura, Jun Ichi
AU - Yoshimura, Akihiko
AU - Oritani, Kenji
AU - Matsuda, Tadashi
N1 - Funding Information:
This study was supported in part by a grant-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The authors declare that they have no conflicts of interest with the contents of this article.
Publisher Copyright:
© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
PY - 2017/11/24
Y1 - 2017/11/24
N2 - 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.
AB - 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.
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U2 - 10.1074/jbc.M117.802884
DO - 10.1074/jbc.M117.802884
M3 - Article
C2 - 28986450
AN - SCOPUS:85035035505
SN - 0021-9258
VL - 292
SP - 19392
EP - 19399
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 47
ER -
