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一种双阴性前列腺癌亚型易受SWI/SNF向降解分子的伤害

Phillip Thienger¹, Irene Paassen², Xiaosai Yao³

¹University of Bern Bern Switzerland.

Cancer research

|January 14, 2026

概括

针对SWI/SNF ATPases的蛋白质溶解向嵌合体 (PROTAC) 疗法在治疗抵抗割的前列腺癌 (CRPC) 中表现有前途. 这些疗法对AR依赖和WNT信号依赖CRPC亚型都有效.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症治疗方法癌症治疗方法

背景情况:

针对SWI/SNF ATPases的蛋白质溶解向嵌合体 (PROTAC) 疗法干扰了依赖AR的割耐性前列腺癌 (CRPC-AR) 中的雄激素受体 (AR) 信号传递.
针对AR阴性CRPC的SWI/SNF向剂的疗效在很大程度上仍未被探索.
具有AR阴性CRPC,特别是WNT信号依赖亚型 (CRPC-WNT),代表着一个重要的未满足的临床需求.

研究的目的:

研究SWI/SNF向剂在AR阴性CRPC中的治疗潜力.
阐明SWI/SNF枯竭影响CRPC-WNT细胞的机制.
为了确定晚期前列腺癌的新疗法策略.

主要方法:

用SWI/SNF向的PROTAC处理CRPC细胞系和有机体模型.
评估细胞活力和信号通路的改变.
耗尽SWI/SNF ATPase SMARCA4并分析其下游目标,包括TCF7L2和MAPK信号.

主要成果:

针对SWI/SNF的PROTAC治疗降低了CRPC-AR和CRPC-WNT细胞的活力.
在CRPC-WNT细胞中的SMARCA4枯竭干扰了转录调节器TCF7L2.2.
发现TCF7L2通过MAPK信号轴维持CRPC-WNT的扩散.

结论:

针对SWI/SNF的疗法对AR依赖CRPC和WNT依赖CRPC都有效.
扰乱TCF7L2的DNA结合或抑制MAPK信号传递是CRPC-WNT的一种可行的治疗策略.
这些发现为晚期前列腺癌的新型治疗方法提供了机制基础.

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