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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN Imprimir: 0893-9675
ISSN On-line: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.2018027913
pages 247-267

Autophagy and Hallmarks of Cancer

Tianzhi Huang
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Xiao Song
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Yongyong Yang
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Xuechao Wan
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Angel A. Alvarez
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Namratha Sastry
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Haizhong Feng
State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
Bo Hu
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
Shi-Yuan Cheng
Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL

RESUMO

Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes.


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