粒体自噬
帕金
细胞生物学
癌细胞
品脱1
生物
线粒体
癌变
自噬
癌症
癌症干细胞
转移
癌症研究
干细胞
遗传学
生物化学
医学
内科学
细胞凋亡
疾病
帕金森病
作者
Debasna P. Panigrahi,Prakash Priyadarshi Praharaj,Chandra Sekhar Bhol,Kewal Kumar Mahapatra,Srimanta Patra,Bishnu Prasad Behera,Soumya Ranjan Mishra,Sujit K. Bhutia
标识
DOI:10.1016/j.semcancer.2019.07.015
摘要
Mitophagy is an evolutionarily conserved cellular process which selectively eliminates dysfunctional mitochondria by targeting them to the autophagosome for degradation. Dysregulated mitophagy results in the accumulation of damaged mitochondria, which plays an important role in carcinogenesis and tumor progression. The role of mitophagy receptors and adaptors including PINK1, Parkin, BNIP3, BNIP3L/NIX, and p62/SQSTM1, and the signaling pathways that govern mitophagy are impaired in cancer. Furthermore, the contribution of mitophagy in regulating the metabolic switch may establish a balance between aerobic glycolysis and oxidative phosphorylation for cancer cell survival. Moreover, ROS-driven mitophagy achieves different goals depending on the stage of tumorigenesis. Mitophagy promotes plasticity in the cancer stem cell through the metabolic reconfiguration for better adaption to the tumor microenvironment. In addition, the present review sheds some light on the role of mitophagy in stemness and differentiation during the transition of cell’s fate, which could have a crucial role in cancer progression and metastasis. In conclusion, this review deals with the detailed molecular mechanisms underlying mitophagy, along with highlighting the dual role of mitophagy in different aspects of cancer, suggesting it as a possible target in the mitophagy-modulated cancer therapy.
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