Mitophagy Receptors in Tumor Biology

Frontiers in Cell and Developmental Biology

Yangchun Xie¹  Rui Kang²  Daolin Tang²  Jiao Liu³ 

[1] Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, China;Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX, United States;The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China;

关键词: mitophagy;    cancer;    cell death;    autophagy;    mitochondria;   

DOI  :  10.3389/fcell.2020.594203

来源: DOAJ

【 摘 要 】

Mitochondria are multifunctional organelles that regulate cancer biology by synthesizing macromolecules, producing energy, and regulating cell death. The understanding of mitochondrial morphology, function, biogenesis, fission and fusion kinetics, and degradation is important for the development of new anticancer strategies. Mitophagy is a type of selective autophagy that can degrade damaged mitochondria under various environmental stresses, especially oxidative damage and hypoxia. The key regulator of mitophagy is the autophagy receptor, which recognizes damaged mitochondria and allows them to enter autophagosomes by binding to MAP1LC3 or GABARAP, and then undergo lysosomal-dependent degradation. Many components of mitochondria, including mitochondrial membrane proteins (e.g., PINK1, BNIP3L, BNIP3, FUNDC1, NIPSNAP1, NIPSNAP2, BCL2L13, PHB2, and FKBP8) and lipids (e.g., cardiolipin and ceramides), act as mitophagy receptors in a context-dependent manner. Dysfunctional mitophagy not only inhibits, but also promotes, tumorigenesis. Similarly, mitophagy plays a dual role in chemotherapy, radiotherapy, and immunotherapy. In this review, we summarize the latest advances in the mechanisms of mitophagy and highlight the pathological role of mitophagy receptors in tumorigenesis and treatment.

【 授权许可】

Unknown