期刊
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 48, 期 1, 页码 60-74出版社
SCIENCE PRESS
DOI: 10.1093/abbs/gmv119
关键词
autophagy; mTOR; breast cancer
资金
- National Institutes of Health [RO1s CA125454, CA188118]
- DOD Breakthrough Award [BC140733P1]
- Mary Kay Ash Foundation
- NATIONAL CANCER INSTITUTE [R01CA125454, R01CA188118, P30CA177558] Funding Source: NIH RePORTER
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.
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