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タイトル: | Experimental evidence of persistent androgen-receptor-dependency in castration-resistant prostate cancer. |
著者: | Kobayashi, Takashi Inoue, Takahiro Kamba, Tomomi Ogawa, Osamu |
著者名の別形: | 小林, 恭 小川, 修 |
キーワード: | prostate cancer castration resistant androgen receptor molecular target |
発行日: | 26-Jul-2013 |
出版者: | MDPI |
誌名: | International journal of molecular sciences |
巻: | 14 |
号: | 8 |
開始ページ: | 15615 |
終了ページ: | 15635 |
抄録: | In the majority of castration-resistant prostate cancer (CRPC), prostate-specific antigen (PSA), product of a gene that is almost exclusively regulated by the androgen receptor (AR), still acts as a serum marker reflecting disease burden, indicating that AR signaling is activated even under castrate level of serum androgen. Accumulated evidence shows that transcriptional ability of AR is activated both in ligand-dependent and -independent manners in CRPC cells. Some androgen-independent sublines derived from originally androgen-dependent LNCaP prostate cancer cells overexpress the AR and PSA, for which silencing the AR gene suppresses cellular proliferation. The overexpression of the AR confers androgen-independent growth ability on androgen-dependent prostate cancer cells. Some patient-derived prostate cancer xenograft lines also acquire castration-resistant growth ability secreting PSA. More recent publications have shown that the AR activated in CRPC cells regulates distinct gene sets from that in androgen-dependent status. This concept provides very important insights in the development of novel anti-prostate cancer drugs such as new generation anti-androgens and CYP17 inhibitors. |
著作権等: | © 2013 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
URI: | http://hdl.handle.net/2433/178033 |
DOI(出版社版): | 10.3390/ijms140815615 |
PubMed ID: | 23896594 |
出現コレクション: | 学術雑誌掲載論文等 |
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