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首頁> 外文期刊>Cancer letters >Preferential induction of G1 arrest in androgen-responsive human prostate cancer cells by androgen receptor signaling antagonists DL3 and antiandrogen bicalutamide.
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Preferential induction of G1 arrest in androgen-responsive human prostate cancer cells by androgen receptor signaling antagonists DL3 and antiandrogen bicalutamide.

機(jī)譯:雄激素受體信號(hào)傳導(dǎo)拮抗劑DL3和抗雄激素比卡魯胺可優(yōu)先誘導(dǎo)雄激素反應(yīng)性人前列腺癌細(xì)胞中G1阻滯。

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摘要

The purpose of this study was to further characterize cell growth-inhibitory effects of a recently identified androgen receptor (AR) signaling inhibitor 6-amino-2-[2-(4-tert-butyl-pnenoxy)-ethylsulfanyl]-1H-pyrimidin-4-one (DL3)(5) and antiandrogen bicalutamide (Bic). DL3 was more potent than Bic in induction of G1 arrest and reduction of G1-related cell cycle protein expression in AR-positive LNCaP cells. DL3, but not Bic, moderately inhibited growth of AR-negative PC-3 cells independent of G1 arrest. The data indicated that DL3 inhibit cell growth in both AR-dependent and -independent manners and is potentially a potent therapeutic agent for the management of advanced human prostate cancer.
機(jī)譯:這項(xiàng)研究的目的是進(jìn)一步表征最近確定的雄激素受體(AR)信號(hào)抑制劑6-氨基-2- [2-(4-叔丁基-苯氧基)-乙基硫基] -1H-嘧啶的細(xì)胞生長(zhǎng)抑制作用-4-one(DL3)(5)和抗雄激素比卡魯胺(Bic)。 DL3比Bic在誘導(dǎo)AR陽性LNCaP細(xì)胞中G1停滯和減少G1相關(guān)細(xì)胞周期蛋白表達(dá)方面更有效。 DL3(而非Bic)可適度抑制AR陰性PC-3細(xì)胞的生長(zhǎng),而與G1阻滯無關(guān)。數(shù)據(jù)表明,DL3以AR依賴性和非依賴性方式抑制細(xì)胞生長(zhǎng),并且潛在地是用于治療晚期人前列腺癌的有效治療劑。

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