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Autophagy and metastasis: another double-edged sword

Candia M Kenific1, Andrew Thorburn, Jayanta Debnath

  • 1Department of Pathology and Diller Comprehensive Cancer Center, University of California San Francisco, CA, United States. Candia.Kenific@ucsf.edu

Current Opinion in Cell Biology
|December 1, 2009
PubMed

Insights

Autophagy, a cellular stress response, has a dual role in cancer metastasis. It can suppress tumor spread by aiding inflammation or restricting growth, but may also promote metastasis by increasing cancer cell survival under stress.

Area of Science:

  • Oncology
  • Cellular Biology
  • Cancer Metastasis

Background:

  • Tumor cells must adapt to stressful microenvironments for metastasis.
  • Autophagy, a cellular self-digestion process, is upregulated during stress.
  • The role of autophagy in metastasis is currently unknown.

Purpose of the Study:

  • To investigate the influence of autophagy on cancer metastasis.
  • To explore the potential prometastatic and antimetastatic roles of autophagy.

Main Methods:

  • The study discusses the known functions and potential roles of autophagy in the context of cellular stress and metastasis.
  • It reviews how autophagy might inhibit or promote tumor cell dissemination and colonization.

Main Results:

  • Autophagy may inhibit metastasis by promoting anti-tumor immunity or limiting dormant tumor cell expansion.
  • Autophagy may promote metastasis by enhancing tumor cell survival against stresses like anoikis.
  • Autophagy's function in metastasis is context-dependent and titratable.

Conclusions:

  • Autophagy exhibits a dual role in cancer metastasis, acting as both a prometastatic and antimetastatic factor.
  • The specific function of autophagy depends on the cellular and environmental demands during the metastatic process.

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