Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 48, Issue 1, Pages 60-74Publisher
SCIENCE PRESS
DOI: 10.1093/abbs/gmv119
Keywords
autophagy; mTOR; breast cancer
Categories
Funding
- 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
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available