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Cancer

A suppression switch

Nature volume 504, pages 225–226 (2013)Cite this article

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The status of the protein p53 determines whether inhibiting the cellular autophagy pathway promotes or inhibits pancreatic cancer in mice. This finding serves as a cautionary tale for clinical trials of autophagy inhibitors. See Letter p.296

Autophagy is a fundamental process in which a cell cannibalizes itself, degrading and recycling cytoplasmic proteins and organelles. This pathway has a crucial role in promoting cellular homeostasis and survival in response to diverse forms of stress, so there is considerable interest in modulating autophagy in cancer cells. So far, clinical trials have focused predominantly on enhancing the efficacy of chemotherapy by inhibiting autophagy, using antimalarial drugs such as hydroxychloroquine1. But there is confusion as to whether inhibiting autophagy enhances or diminishes cancer therapy — current evidence suggests that both may be true. In this issue, Rosenfeldt et al.2 (page 296) identify the tumour-suppressor protein p53 as a determinant of whether autophagy suppresses or accelerates the progression of pancreatic cancer.

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Figure 1: Autophagy, p53 and cancer progression.

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Authors and Affiliations

  1. Hanna Starobinets and Jayanta Debnath are in the Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco 94143, USA.,

    Hanna Starobinets & Jayanta Debnath

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  1. Hanna Starobinets
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  2. Jayanta Debnath
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Correspondence to Jayanta Debnath.

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Starobinets, H., Debnath, J. A suppression switch. Nature 504, 225–226 (2013). https://doi.org/10.1038/nature12841

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