Autophagy regulation in the development and treatment of breast cancer

• Published in: Acta biochimica et biophysica Sinica 2016-01, Vol.48 (1), p.60-74
• Main Authors: Zhou, Yuting, Rucker, 3rd, Edmund B, Zhou, Binhua P
• Format: Article
• Language: English
• Subjects: Animals; Antineoplastic Agents - chemistry; Autophagy; Beclin-1 - metabolism; Breast Neoplasms - drug therapy; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Cell Survival; Gene Expression Regulation, Neoplastic; Genotype; Humans; Inflammation; Lysosomes - metabolism; Mice; Neoplasm Metastasis; Phenotype; Phosphatidylinositol 3-Kinases - metabolism; Reviews; Signal Transduction; 乳腺癌; 治疗效果; 细胞类型; 肿瘤转移; 自噬; 蛋白质复合物; 调控; 调节机制
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmv119

Autophagy is a major catabolic process in which intracellular membrane structures, protein com- plexes, and lysosomes are formed as lysoautophagosome to degrade and renew cytoplasmic com- ponents. 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 patho- logical 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.