雌激素受体及其蛋白相互作用体在抵抗割的前列腺癌中的演变作用
Muj Chukhu1, Ujjwal R Dahiya1, Hannelore V Heemers2
1Department of Cancer Biology, Cleveland Clinic Research, Cleveland Clinic, Cleveland, OH, USA.
雄激素受体 (AR) 驱动前列腺癌 (CaP) 的进展. 除了转录之外,AR影响RNA剪接和翻译,有助于治疗耐药性和攻击性CaP. 针对AR交互器提供了新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 雄激素受体 (AR) 是致命前列腺癌 (CaP) 进展的关键驱动因素.
- 基剥夺疗法 (ADT) 是标准的治疗方法,但耐药性 (CRPC) 最终会发展.
- CRPC通常仍然依赖于AR,依赖于AR的生长活动.
研究的目的:
- 审查和对比AR在CaP进展中的独特功能.
- 探索AR的非传统的转录和转录独立的角色.
- 讨论针对AR - 核心调节器相互作用的新型CaP治疗策略的含义.
主要方法:
- 文献综述和分析CAP中的AR功能.
- 对AR的转录和非转录作用的对比.
- 评估AR相互作用蛋白及其作用.
主要成果:
- AR的作用超出了联体激活转录的范围.
- AR影响非编码RNA,拼接和翻译,从而导致耐药性.
- 增强现实交互器参与各种依赖于增强现实的过程.
结论:
- AR的多方面的作用对CaP的进展和抵抗至关重要.
- 了解AR的非转录功能对于开发新疗法至关重要.
- 准AR-coregulator相互作用可能会克服ADT抵抗.
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