在LKB1-缺陷KRAS驱动的肺癌中,G6PD维持了再氧化恒温和生物合成
Taijin Lan1,2, Sara Arastu1, Samuel Wang1
1Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08901, USA.
bioRxiv : the preprint server for biology
|October 24, 2023
概括
葡萄糖-6-酸盐脱酶 (G6PD) 推动了癌细胞的生长. 抑制G6PD可以通过影响NADPH的产生和激活p53.3来抑制KRAS;LKB1肺瘤.
科学领域:
- 在瘤学瘤学.
- 代谢途径 代谢途径
- 癌细胞的新陈代谢
背景情况:
- 癌细胞需要尼古丁胺胺氨基二核酸盐 (NADPH) 进行氧化还原平衡和生物合成.
- 通过葡萄糖-6-酸脱酶 (G6PD) 的氧化酸途径是NADPH的主要来源.
- 替代的NADPH通路可以补偿某些癌症中的G6PD损失.
结论:
- 致癌驱动突变决定了癌细胞对G6PD的依赖.
- 针对G6PD为KRAS和LKB1共变肺癌提供了潜在的治疗策略.
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