Interaction between docetaxel resistance and castration resistance in prostate cancer: Implications of twist1, YB-1, and androgen receptor

多西紫杉醇 紫杉烷 前列腺癌 LNCaP公司 雄激素受体 医学 癌症研究 雄激素剥夺疗法 内科学 肿瘤科 基因敲除 癌细胞 癌症 生物 乳腺癌 细胞凋亡 生物化学
作者
Masaki Shiota,Eiji Kashiwagi,Akira Yokomizo,Ario Takeuchi,Takashi Dejima,Yu Song,Katsunori Tatsugami,Junichi Inokuchi,Takeshi Uchiumi,Seiji Naito
出处
期刊:The Prostate [Wiley]
卷期号:73 (12): 1336-1344 被引量:50
标识
DOI:10.1002/pros.22681
摘要

Taxanes, including docetaxel, are currently the only cytotoxic chemotherapeutic agents proven to confer survival benefit in patients with castration-resistant prostate cancer (CRPC). However, the merits of taxanes remain modest, and efforts are needed to improve their therapeutic efficacy.We evaluated the sensitivity of prostate cancer cells to various agents using cytotoxicity assays. Gene and protein expression levels were evaluated by quantitative real-time polymerase chain reaction and Western blotting analysis, respectively.Hydrogen peroxide-resistant and castration-resistant cells that overexpressed Twist1 and Y-box binding protein-1 (YB-1) were cross-resistant to cytotoxic agents, including docetaxel. Twist1 regulated YB-1 expression in prostate cancer cells, supported by the induction of Twist1 and YB-1 by transforming-growth factor-β, which is critical for taxane resistance. Twist1 and/or YB-1 were activated in docetaxel-resistant prostate cancer cells, and YB-1 was activated by docetaxel treatment. Conversely, Twist1 and YB-1 knockdown sensitized prostate cancer cells to cytotoxic agents, including docetaxel. In addition, androgen receptor (AR) knockdown increased cellular sensitivity to docetaxel, though AR expression in docetaxel-resistant LNCaP cells was paradoxically lower than in parental cells. Intriguingly, androgen deprivation treatment was more effective in docetaxel-resistant LNCaP cells compared with parental cells.Twist1/YB-1 and AR signaling promote docetaxel resistance in CRPC cells. However, docetaxel-resistant cells were collaterally sensitive to androgen deprivation because of down-regulation of AR expression, suggesting that the therapeutic effect of initial taxane treatment in hormone-naïve prostate cancer may be superior to that of salvage taxane treatment in CRPC.
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