@article{oai:shiga-med.repo.nii.ac.jp:00003873,
 author = {佐藤, 朗 and 清水, 昭男 and 米野, 雅大 and 和田, 晃典 and 河内, 明宏 and 扇田, 久和 and RAHMAN, Nor Idayu A. and SATO, Akira and TSEVELNOROV, Khurelbaatar and SHIMIZU, Akio and KOMENO, Masahiro and AHMAT AMIN, Mohammad Khusni Bin and MOLLA, Md Rasel and SOH, Joanne Ern Chi and NGUYEN, Le Kim Chi and WADA, Akinori and KAWAUCHI, Akihiro and 扇田, 久和},
 issue = {9},
 journal = {Cancer research},
 month = {May},
 note = {The growth and progression of cancers are crucially regulated by the tumor microenvironment where tumor cells and stromal cells are mutually associated. In this study, we found that stomatin expression was markedly upregulated by the interaction between prostate cancer cells and stromal cells. Stomatin suppressed cancer cell proliferation and enhanced apoptosis in vitro and inhibited xenograft tumor growth in vivo. Stomatin inhibited Akt activation, which is mediated by phosphoinositide-dependent protein kinase 1 (PDPK1). PDPK1 protein stability was maintained by its binding to HSP90. Stomatin interacted with PDPK1 and interfered with the PDPK1-HSP90 complex formation, resulting in decreased PDPK1 expression. Knockdown of stomatin in cancer cells elevated Akt activation and promoted cell increase by promoting the interaction between PDPK1 and HSP90. Clinically, stomatin expression levels were significantly decreased in human prostate cancer samples with high Gleason scores, and lower expression of stomatin was associated with higher recurrence of prostate cancer after the operation. Collectively, these findings demonstrate the tumor-suppressive effect of stromal-induced stomatin on cancer cells. SIGNIFICANCE: These findings reveal that interactions with stromal cells induce expression of stomatin in prostate cancer cells, which suppresses tumor growth via attenuation of the Akt signaling axis., Journal Article},
 pages = {2318--2331},
 title = {Stomatin-Mediated Inhibition of the Akt Signaling Axis Suppresses Tumor Growth.},
 volume = {81},
 year = {2021}
}