Autophagy as a therapeutic target in cancer

被引:289
作者
Chen, Ning [1 ,2 ,3 ]
Karantza, Vassiliki [2 ,3 ]
机构
[1] Univ Med & Dent New Jersey, Dept Internal Med, Div Med Oncol, Piscataway, NJ 08854 USA
[2] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA
[3] Canc Inst New Jersey, New Brunswick, NJ USA
关键词
autophagy; tumorigenesis; chemotherapy; radiation; cancer treatment; HISTONE DEACETYLASE INHIBITOR; ACTIVATED PROTEIN-KINASE; MALIGNANT GLIOMA-CELLS; TUMOR-SUPPRESSOR GENE; INDUCED APOPTOSIS; ARSENIC TRIOXIDE; COMBINATION TREATMENT; INDUCED CYTOTOXICITY; REGULATES AUTOPHAGY; PIK3CA MUTATIONS;
D O I
10.4161/cbt.11.2.14622
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Autophagy is a self-catabolic process that maintains intracellular homeostasis and prolongs cell survival under stress via lysosomal degradation of cytoplasmic constituents and recycling of amino acids and energy. Autophagy is intricately involved in many aspects of human health and disease, including cancer. Autophagy is a double-edged sword in tumorigenesis, acting both as a tumor suppressor and a protector of cancer cell survival, and elucidation of its exact role at different stages of cancer progression and in treatment responsiveness is a complex and challenging task. Better understanding of autophagy regulation and its impact on treatment outcome will potentially allow us to identify novel therapeutic targets in cancer. In this review, we summarize current knowledge on the regulation and dual function of autophagy in tumorigenesis, as well as ongoing efforts in modulating autophagy for cancer treatment and prevention. This is a very exciting and highly promising area of cancer research, as pharmacologic modulation of autophagy appears to augment the efficacy of currently available anticancer regimens and opens the way to the development of new combinatorial therapeutic strategies that will hopefully contribute to cancer eradication.
引用
收藏
页码:157 / 168
页数:12
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