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通过细胞命运转换,RAD51B-EZH2轴作为TNBC的潜在治疗点

Shiqi Lin^1,2,3, Dongyang Tang^1,2, Josh Haipeng Lei^1,2

¹MOE Frontier Science Center for Precision Oncology, University of Macau, Macau SAR, China.

Cell death & disease

|November 29, 2025

概括

三阴性乳腺癌 (TNBC) 是具有攻击性的,缺乏目标. 缺少Rad51b会抑制ERα,从而产生TNBC. 针对RAD51B-EZH2轴重新表达ERα,使TNBC可通过内分泌疗法治疗.

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:

三阴性乳腺癌 (TNBC) 是一种具有有限治疗点的侵袭性亚型.
识别新型分子驱动因素对于开发TNBC有效治疗至关重要.

研究的目的:

为了确定参与TNBC形成的候选驱动基因.
阐明TNBC发展背后的分子机制,并确定潜在的治疗点.

主要方法:

在小鼠模型 (Brca1缺乏和Fgfr2突变) 中使用睡眠美女 (SB) 转位子系统进行功能查.
研究了Rad51b缺乏在TNBC发育和ERα抑制中的作用.
分析了Polycomb Repressive Complex 2 (PRC2) 的参与,组织蛋白修饰和AMPK通路.

主要成果:

确定了64个重叠的候选驱动基因用于TNBC诱导.
证明Rad51b缺陷通过PRC2招募和H3K27三甲基化抑制雌激素受体α (ERα) 表达.
表明RAD51B的损失可提高ATP的调节,抑制AMPK,并降低EZH2的酸化,从而增强PRC2的活动并抑制Esr1.

结论:

RAD51B-EZH2轴是TNBC中ERα表达的关键调节者.
抑制这一轴可以恢复ERα的表达,使TNBC易受内分泌治疗.
结合EZH2抑制剂和他莫西芬的联合治疗在减少TNBC进展方面显示出有前途.

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