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Nat Commun: BCL-XL直接调节RAS有利于癌细胞获得干细胞属性

2017-11-02 MedSci MedSci原创

肿瘤组织中,表达高水平抗凋亡蛋白(例如BCL-XL)的化学抗性细胞的积累被认为是在进展和/或初始治疗期间对敏感的低表达克隆进行反选择的结果。本研究中,研究人员发现,即使在没有促凋亡压力的情况下,BCL-XL表达选择性地有利于癌细胞群体。在转化的人乳腺上皮细胞中,BCL-XL有利于组合型活性RAS的下游信号的完全激活,以BH4依赖性的方式相互作用。对比蛋白质组学分析和功能测定表明,这对RAS诱导的干

肿瘤组织中,表达高水平抗凋亡蛋白(例如BCL-XL)的化学抗性细胞的积累被认为是在进展和/或初始治疗期间对敏感的低表达克隆进行反选择的结果。

本研究中,研究人员发现,即使在没有促凋亡压力的情况下,BCL-XL表达选择性地有利于癌细胞群体。在转化的人乳腺上皮细胞中,BCL-XL有利于组合型活性RAS的下游信号的完全激活,以BH4依赖性的方式相互作用。对比蛋白质组学分析和功能测定表明,这对RAS诱导的干细胞调节物的表达和维持癌症起始细胞(CIC)表型至关重要。

因此,耐药性癌细胞来自于RAS诱导的自我更新的BCL-XL调节驱动的阳性选择,其中凋亡耐药不一定是直接选择的特征。

原始出处:


Sophie de Carné Trécesson, Frédérique Souazé, et al., BCL-XL directly modulates RAS signalling to favour cancer cell stemness. Nat Commun. 2017; 8: 1123. Published online 2017 Oct 24. doi: 10.1038/s41467-017-01079-1

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    2018-07-25 liye789132251
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    2018-07-28 liuli5079
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