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阐明分子分层单剂和组合治疗策略,针对致命前列腺癌的MCL1

Juan M Jiménez-Vacas¹, Daniel Westaby^1,2, Ines Figueiredo¹

¹The Institute of Cancer Research, London, UK.

Nature communications

|October 8, 2025

概括

向抗亡蛋白质MCL1对转移性割抵抗性前列腺癌 (mCRPC) 显示出希望. 抑制MCL1或与AKT抑制剂的联合治疗为mCRPC患者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
癌症治疗方法癌症治疗方法

背景情况:

转移性割抵抗性前列腺癌 (mCRPC) 需要新的治疗方法.
抗亡蛋白MCL1与癌细胞存活有关,但其在mCRPC中的作用尚不清楚.

研究的目的:

在mCRPC中描述MCL1并评估MCL1抑制的有效性.
探索涉及特定mCRPC亚型的MCL1和AKT抑制的组合疗法.

主要方法:

在mCRPC活检队列和患者衍生模型中分析MCL1.
评估MCL1抑制和MCL1/AKT联合抑制的抗瘤作用.
研究分子相互作用 (BAD-BCLXL,BIM-MCL1) 和抵抗机制.

主要成果:

增加MCL1拷贝数 (14%-34%) 与增加的MCL1表达和mCRPC的较差结果有关.
在获得MCL1的mCRPC模型中,MCL1抑制显示出抗瘤活性.
在PTEN损失/PI3K激活模型中,MCL1和AKT的联合抑制诱导了癌症特异性细胞死亡,克服了对AKT抑制剂的获得性耐药性.

结论:

在mCRPC中,MCL1是可行的治疗点,特别是在MCL1增长的情况下.
与MCL1和AKT抑制剂的联合治疗显示出PTEN损失/PI3K激活mCRPC的潜力.
这些发现支持MCL1向治疗在mCRPC中的临床转化.

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