The double-edged sword of autophagy modulation in cancer

Eileen White, Robert S. DiPaola

Research output: Contribution to journalReview articlepeer-review

871 Scopus citations

Abstract

Macroautophagy (autophagy) is a lysosomal degradation pathway for the breakdown of intracellular proteins and organelles. Although constitutive autophagy is a homeostatic mechanism for intracellular recycling and metabolic regulation, autophagy is also stress responsive, in which it is important for the removal of damaged proteins and organelles. Autophagy thereby confers stress tolerance, limits damage, and sustains viability under adverse conditions. Autophagy is a tumor-suppression mechanism, yet it enables tumor cell survival in stress. Reconciling how loss of a prosurvival function can promote tumorigenesis, emerging evidence suggests that preservation of cellular fitness by autophagy may be key to tumor suppression. As autophagy is such a fundamental process, establishing how the functional status of autophagy influences tumorigenesis and treatment response is important. This is especially critical as many current cancer therapeutics activate autophagy. Therefore, efforts to understand and modulate the autophagy pathway will provide new approaches to cancer therapy and prevention.

Original languageEnglish
Pages (from-to)5308-5316
Number of pages9
JournalClinical Cancer Research
Volume15
Issue number17
DOIs
StatePublished - Sep 1 2009

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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