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Your search keyword '"Hanaki, Shunsuke"' showing total 12 results
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12 results on '"Hanaki, Shunsuke"'

8. FKBP52 and FKBP51 differentially regulate the stability of estrogen receptor in breast cancer

Author

Habara, Makoto, primary, Sato, Yuki, additional, Goshima, Takahiro, additional, Sakurai, Masashi, additional, Imai, Hiroyuki, additional, Shimizu, Hideyuki, additional, Katayama, Yuta, additional, Hanaki, Shunsuke, additional, Masaki, Takahiro, additional, Morimoto, Masahiro, additional, Nishikawa, Sayaka, additional, Toyama, Tatsuya, additional, and Shimada, Midori, additional

Published
2022
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12. FKBP51 and FKBP52 regulate androgen receptor dimerization and proliferation in prostate cancer cells.

Author

Maeda K, Habara M, Kawaguchi M, Matsumoto H, Hanaki S, Masaki T, Sato Y, Matsuyama H, Kunieda K, Nakagawa H, and Shimada M

Subjects
Cell Proliferation, Dimerization, Humans, Male, Tacrolimus Binding Proteins genetics, Tacrolimus Binding Proteins metabolism, Prostatic Neoplasms genetics, Prostatic Neoplasms metabolism, Receptors, Androgen metabolism
Abstract

The growth of prostate cancer is dependent on the androgen receptor (AR), which serves as a ligand-specific transcription factor. Although two immunophilins, FKBP51 and FKBP52, are known to regulate AR activity, the precise mechanism remains unclear. We found that depletion of either FKBP51 or FKBP52 reduced AR dimer formation, chromatin binding, and phosphorylation, suggesting defective AR signaling. Furthermore, the peptidyl-prolyl cis/trans isomerase activity of FKBP51 was found to be required for AR dimer formation and cancer cell growth. Treatment of prostate cancer cells with FK506, which binds to the FK1 domain of FKBPs, or with MJC13, an inhibitor of FKBP52-AR signaling, also inhibited AR dimer formation. Finally, elevated expression of FKBP52 was associated with a higher rate of prostate-specific antigen recurrence in patients with prostate cancer. Collectively, these results suggest that FKBP51 and FKBP52 might be promising targets for prostate cancer treatment through the inhibition of AR dimer formation., (© 2021 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.)

Published
2022
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