自噬
细胞生物学
癌变
细胞凋亡
细胞器
程序性细胞死亡
生物
细胞内
炎症
平衡
癌细胞
溶酶体
癌症
癌症研究
免疫学
生物化学
酶
遗传学
作者
Robin Mathew,Vassiliki Karantza‐Wadsworth,Eileen White
摘要
Cells with defects in the autophagic pathway are sensitized to apoptosis in response to metabolic stress, but, paradoxically, autophagy defects are associated with increased tumorigenesis. How can this paradox be resolved? Autophagy is a cellular degradation pathway for the clearance of damaged or superfluous proteins and organelles. The recycling of these intracellular constituents also serves as an alternative energy source during periods of metabolic stress to maintain homeostasis and viability. In tumour cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the mechanism behind this has not been determined. Recent evidence suggests that autophagy provides a protective function to limit tumour necrosis and inflammation, and to mitigate genome damage in tumour cells in response to metabolic stress.
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