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在癌症干细胞丰富方面,ALDH2功能障碍和酒精合作

Samuel Flashner¹, Masataka Shimonosono¹, Yasuto Tomita¹

¹Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, Columbia University, New York, NY 10032, USA.

|November 18, 2023

概括

酒精代谢功能障碍通过增加癌症干细胞和促进对化疗的耐药性来加速食道癌症. 这突出了乙甲.

科学领域:

在瘤学瘤学.
遗传学遗传学是一个
生物化学生物化学

背景情况:

乙甲是一种酒精代谢物,是人类致癌物,与食道状细胞癌 (ESCC) 有关.
化脱酶2 (ALDH2) 排毒乙;它的功能障碍,特别是东亚人中常见的ALDH2*2变体,增加了ESCC风险.
通过ALDH2功能障碍驱动ESCC病理生物学的确切机制尚不清楚.

研究的目的:

研究在ALDH2功能障碍条件下,ESCC和新生细胞如何对酒精暴露做出反应.
阐明ALDH2功能障碍在癌症干细胞丰富和ESCC治疗抵抗中的作用.

主要方法:

利用细胞系,3D有机体和异种移植模型来研究酒精暴露的影响.
评估了癌症干细胞标记物 (CD44H),活性氧物种,DNA损伤和亡.
研究了ALDH2激活 (Alda-1) 和西斯治疗对细胞反应的影响.

主要成果:

与ALDH2*2相结合的酒精暴露显著增加了CD44H癌症干细胞,促进瘤开始和治疗耐药性.
ALDH2*2加剧了酒精诱导的氧化应激和DNA损伤,导致非干细胞的亡.
艾尔达-1治疗逆转了这些影响,证实了乙甲是主要的驱动因素.
ALDH2 功能障碍促进了 cisplatin 治疗后的 CD44H 细胞丰富,这表明了对 cisplatin 耐药性的机制.

结论:

通过丰富CD44H癌症干细胞,ALDH2功能障碍加速ESCC的发病过程.
这种丰富是由基因毒性压力因素驱动的,包括环境致癌物和化疗剂.
结果提供了对ESCC发展和潜在的针对ALDH2功能的治疗策略的见解.

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