Autophagy regulation in the development and treatment of breast cancer

Acta Biochim Biophys Sin (Shanghai). 2016 Jan;48(1):60-74. doi: 10.1093/abbs/gmv119. Epub 2015 Dec 5.

Abstract

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.

Keywords: autophagy; breast cancer; mTOR.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • 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
  • Signal Transduction

Substances

  • Antineoplastic Agents
  • BECN1 protein, human
  • Beclin-1
  • Phosphatidylinositol 3-Kinases