Autophagy in cancer metastasis

被引:373
|
作者
Mowers, E. E. [1 ,2 ]
Sharifi, M. N. [1 ,3 ,4 ]
Macleod, K. F. [1 ,4 ]
机构
[1] Univ Chicago, Ben May Dept Canc Res, 929 East 57th St GCIS W338, Chicago, IL 60422 USA
[2] Univ Chicago, Interdisciplinary Scientist Training Program, Chicago, IL 60637 USA
[3] Univ Chicago, Med Scientist Training Program, Chicago, IL USA
[4] Univ Chicago, Comm Canc Biol, Chicago, IL 60637 USA
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; FOCAL ADHESION KINASE; HYPOXIA-INDUCED AUTOPHAGY; SUPPRESSOR GENE ARHI; BREAST-CANCER; EXTRACELLULAR-MATRIX; STEM-CELLS; OVARIAN-CANCER; TUMOR-CELLS; BONE-MARROW;
D O I
10.1038/onc.2016.333
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1619 / 1630
页数:12
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