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Autophagy

Exploring the anticancer effects of autophagy inhibition

Nature Reviews Cancer volume 15, pages 512–513 (2015)Cite this article

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Autophagy, an important process in homeostasis that involves the lysosomal degradation and recycling of cellular components, has been shown to promote tumour growth and progression in some tissues. Lévy et al. now reveal that autophagy is abnormally active during colorectal cancer (CRC) development and is required for cancer cell metabolism.

The authors investigated the status of autophagy in intestinal epithelial cells (IECs) during tumorigenesis in adenomatous polyposis coli (Apc) conditional knockout mice. To that end, they analysed the levels of p62 (also known as sequestosome 1), a protein that targets specific cellular components for autophagy; p62 levels were lower in Apc+/− tumoural tissue than in non-tumoural tissue. They also analysed the presence of autophagolysosomes and the expression of key autophagy-related (ATG) genes. ATG genes were expressed not only in Apc+/− mice but also in around 20% of human samples during all stages of CRC. Deletion of Atg7, which is essential for the biogenesis of autophagolysosomes, in IECs in the Apc+/− mice inhibited the tumorigenic process. Apc+/−Atg7−/− mice showed fewer colonic tumours than Apc+/− mice, and these tumours were much smaller and developed more slowly than those in Apc+/− mice.

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References

  1. Lévy, J. et al. Intestinal inhibition of Atg7 prevents tumour initiation through a microbiome-influenced immune response and suppresses tumour growth. Nat. Cell Biol. 17, 1062–1073 (2015)

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  1. M. Teresa Villanueva
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Villanueva, M. Exploring the anticancer effects of autophagy inhibition. Nat Rev Cancer 15, 512–513 (2015). https://doi.org/10.1038/nrc4003

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