Expanding perspectives on the significance of mitophagy in cancer. (December 2017)

• Record Type: Journal Article
• Authors: Drake, Lauren E.; Springer, Maya Z.; Poole, Logan P.; Kim, Casey J.; Macleod, Kay F.
• Is Part Of: Seminars in cancer biology. Volume 47(2017)
• Page Start: 110
• Page End: 124
• Publication Date: 2017-12
• Subjects: ALS amyotrophic lateral sclerosis -- AR androgen receptor -- ASC apoptosis-associated speck-like protein containing a CARD -- ATM ataxia telangiectasia mutated -- BCL-2 breakpoint cluster locus-2 -- BCL-XL BCL2-like 1 long -- BNIP3 BCL2 interacting protein 3 -- BNIP3L BCL2 interacting protein 3 like -- BRCA1 breast cancer 1 -- CCCP carbonyl cyanide 3-chlorophenylhydrazone -- CK2 casein kinase-2 -- CL cardiolipin -- DRP1 dynamin related protein 1 -- ETC electron transport chain -- FA Fanconi anemia -- FANC-C FA protein C -- FUNDC1 FUN 14 domain containing 1 -- GAP GTPase activating protein -- GDI GDP dissociation inhibitor -- HCC hepatocellular carcinoma -- IMM inner mitochondrial membrane -- IRF3 interferon response factor 3 -- LC3 microtubule associated protein 1 light chain 3 -- LIR LC3 interacting region -- mtDNA mitochondrial DNA -- MAVS mitochondrial anti-viral signaling protein -- MFN mitofusin -- NBR1 near BRCA1 -- NDP52 nuclear dot protein 52 -- NLRP3 nucleotide binding domain and leucine rich repeat pyrin domain containing 3 -- NSCLC non-small cell lung carcinoma -- OMM outer mitochondrial membrane -- OPTN optineurin, p62/SQSTM1 -- PARK2 Parkin encoding locus -- PARK6 PINK1 encoding locus -- PARK8 LRRK2 encoding locus -- PD Parkinson's disease -- PDAC pancreatic ductal adenocarcinoma -- PGAM5 phosphoglycerate mutase family member 5 -- PHB-2 prohibitin-2 -- PINK1 PTEN induced putative kinase 1 -- PLK1 Polo-like kinase-1 -- ROS reactive oxygen species -- SRC Rous sarcoma oncogene -- TAX1BP1 Tax1 binding protein 1 -- TAZ tafazzin -- TBK TANK binding kinase 1 -- ULK1 Unc-51-like autophagy activating kinase 1; Mitochondria -- Mitophagy -- Biogenesis -- Parkin -- BNIP3/BNIP3L -- FUNDC1 -- Cardiolipin -- Metabolic reprogramming -- Cell fate determination -- Inflammasome activation -- DNA damage responses; Cancer -- Periodicals; Neoplasms -- Periodicals; Review Literature; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.semcancer.2017.04.008
• Languages: English
• ISSNs: 1044-579X

Abstract

Abstract: Mitophagy is a selective mode of autophagy in which mitochondria are specifically targeted for degradation at the autophagolysosome. Mitophagy is activated by stresses such as hypoxia, nutrient deprivation, DNA damage, inflammation and mitochondrial membrane depolarization and plays a role in maintaining mitochondrial integrity and function. Defects in mitophagy lead to mitochondrial dysfunction that can affect metabolic reprogramming in response to stress, alter cell fate determination and differentiation, which in turn affects disease incidence and etiology, including cancer. Here, we discuss how different mitophagy adaptors and modulators, including Parkin, BNIP3, BNIP3L, p62/SQSTM1 and OPTN, are regulated in response to physiological stresses and deregulated in cancers. Additionally, we explore how these different mitophagy control pathways coordinate with each other. Finally, we review new developments in understanding how mitophagy affects stemness, cell fate determination, inflammation and DNA damage responses that are relevant to understanding the role of mitophagy in cancer.