Autophagy regulation in the development and treatment of breast cancer

被引:46
作者
Zhou, Yuting [1 ,3 ]
Rucker, Edmund B., III [2 ,3 ]
Zhou, Binhua P. [1 ,3 ]
机构
[1] Univ Kentucky, Sch Med, Dept Mol & Cellular Biochem, Lexington, KY 40506 USA
[2] Univ Kentucky, Coll Arts & Sci, Dept Biol, Lexington, KY 40506 USA
[3] Univ Kentucky, Sch Med, Dept Markey Canc Ctr, Lexington, KY 40506 USA
基金
美国国家卫生研究院;
关键词
autophagy; mTOR; breast cancer; BCL-X-L; CELL-DEATH; TRANSGENIC MICE; APOPTOSIS; BECLIN-1; PROTEIN; TARGET; INHIBITION; COMPLEX; GENE;
D O I
10.1093/abbs/gmv119
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy is a major catabolic process in which intracellular membrane structures, protein complexes, and lysosomes are formed as lysoautophagosome to degrade and renew cytoplasmic components. Autophagy is physiologically a strategy and mechanism for cellular homeostasis as well as adaptation to stress, and thus alterations in the autophagy machinery may lead to diverse pathological conditions. The role of autophagy in cancer is complex, and the current literature reflects this as a 'double-edged sword'. Autophagy shows promise as a novel therapeutic target in various types of breast cancer, inhibiting or increasing treatment efficacy in a context- and cell-type-dependent manner. This review aims to summarize the recent advances in the understanding of the mechanisms by which key modulators of autophagy participate in cancer metastasis, highlight different autophagy-deficient murine models for breast cancer study, and provide further impetus for the modulation of autophagy in anticancer therapy.
引用
收藏
页码:60 / 74
页数:15
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