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Autophagy Regulates Stress Responses, Metabolism, and Anticancer Immunity
被引:77
|作者:
White, Eileen
[1
,2
,6
]
Lattime, Edmund C.
[1
,3
]
Guo, Jessie Yanxiang
[1
,4
,5
]
机构:
[1] Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA
[2] Rutgers State Univ, Dept Mol Biol & Biochem, Piscataway, NJ 08854 USA
[3] Rutgers State Univ, Robert Wood Johnson Med Sch, Dept Surg, New Brunswick, NJ USA
[4] Rutgers State Univ, Robert Wood Johnson Med Sch, Dept Med, New Brunswick, NJ USA
[5] Rutgers Ernest Mario Sch Pharm, Dept Chem Biol, Piscataway, NJ USA
[6] Princeton Univ, Ludwig Princeton Branch, Ludwig Inst Canc Res, Princeton, NJ 08544 USA
来源:
关键词:
TUMOR;
GLUCOSE;
GROWTH;
NRF2;
D O I:
10.1016/j.trecan.2021.05.003
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Autophagy is a catabolic intracellular nutrient-scavenging pathway triggered by nutrient deprivation and stress that captures and degrades intracellular proteins and organelles in lysosomes. The breakdown products are then recycled into metabolic pathways to sustain survival. Organelle turnover by autophagy contributes to quality control and suppresses inflammation. Autophagy is upregulated in many cancers and supports their growth, survival, and malignancy in a tumor cell-autonomous fashion. Host autophagy also promotes tumor growth by maintaining a supply of essential nutrients and suppressing innate and adaptive antitumor immune responses. Autophagy is also upregulated in response to cancer therapy and confers treatment resistance. Thus, autophagy is a cancer vulnerability and its inhibition is under investigation as a novel therapeutic approach.
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页码:778 / 789
页数:12
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