Journal
BIOLOGICAL REVIEWS
Volume 93, Issue 1, Pages 152-165Publisher
WILEY
DOI: 10.1111/brv.12337
Keywords
autophagy; cancer; cancer stem cells; oxidative stress; therapy
Categories
Funding
- Instituto de Salud Carlos III [PI12/01104, PI15/01262]
- European Regional Development Fund (ERDF)
- Marie Curie - COFUND program, Spain [INCOMED - GA 267128]
- Vall d'Hebron Institut de Recerca (VHIR)
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In wild-type cells, autophagy represents a tumour-suppressor mechanism, and dysfunction of the autophagy machinery increases genomic instability, DNA damage, oxidative stress and stem/progenitor expansion, which are events associated with cancer onset. Autophagy occurs at a basal level in all cells depending on cell type and cellular microenvironment. However, the role of autophagy in cancer is diverse and can promote different outcomes even in a single tumour. For example, in hypoxic tumour regions, autophagy emerges as a protective mechanism and allows cancer cell survival. By contrast, in cancer cells surrounding the tumour mass, the induction of autophagy by radio- or chemotherapy promotes cell death and significantly reduces the tumour mass. Importantly, inhibition of autophagy compromises tumorigenesis by mechanisms that are not entirely understood. The aim of this review is to explain the apparently contradictory role of autophagy as a mechanism that both promotes and inhibits tumorigenesis using different models. The induction/inhibition of autophagy as a mechanism for cancer treatment is also discussed.
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