Autophagy in cancer metastasis.
Autophagy is a highly conserved self-degradative process that has a key role in cellular stress responses and survival. Recent work has begun to explore the function of autophagy in cancer metastasis, which is of particular interest given the dearth of effective therapeutic options for metastatic disease. Autophagy is induced upon progression of various human cancers to metastasis and together with data from genetically engineered mice and experimental metastasis models, a role for autophagy at nearly every phase of the metastatic cascade has been identified. Specifically, autophagy has been shown to be involved in modulating tumor cell motility and invasion, cancer stem cell viability and differentiation, resistance to anoikis, epithelial-to-mesenchymal transition, tumor cell dormancy and escape from immune surveillance, with emerging functions in establishing the pre-metastatic niche and other aspects of metastasis. In this review, we provide a general overview of how autophagy modulates cancer metastasis and discuss the significance of new findings for disease management.
The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA.|Inter-disciplinary Scientist Training Program, The University of Chicago, Chicago, IL, USA.
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Mowers
The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA.|Medical Scientist Training Program, The University of Chicago, Chicago, IL, USA.|The Committee on Cancer Biology, The University of Chicago, Chicago, IL, USA.
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Sharifi
The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA.|The Committee on Cancer Biology, The University of Chicago, Chicago, IL, USA.
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Macleod
D000818:Animals; D023102:Anoikis / Q000235:genetics; D001343:Autophagy / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics; D002465:Cell Movement / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D007157:Immunologic Surveillance; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000209:etiology* / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D014411:Neoplastic Stem Cells / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D019139:Tumor Escape / Q000235:genetics / Q000276:immunology; D059016:Tumor Microenvironment / Q000235:genetics / Q000276:immunology