生物
重编程
克拉斯
胆固醇
肺癌
囤积(动物行为)
癌症研究
突变体
癌症
肺
生物发生
细胞生物学
细胞
生物信息学
内科学
内分泌学
遗传学
医学
基因
结直肠癌
摄食行为
标识
DOI:10.1016/j.stem.2023.05.006
摘要
Proliferative cells require excess cholesterol to support rapid membrane biogenesis. Using a mutant KRAS mouse model of non-small cell lung cancer, Guilbaud et al. show that lung cancers accumulate cholesterol by locally and distally reprogramming lipid trafficking and that cholesterol-removing interventions may hold promise as a therapeutic strategy.
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