title: Dysregulation of mitophagy in carcinogenesis and tumor progression.
abstract: The mitochondrial role in carcinogenesis and cancer progression is an area of active research, with many unresolved questions. Various aspects of altered mitochondrial function have been implicated in tumorigenesis and tumor progression, including mitochondrial dysfunction, a metabolic switch to aerobic glycolysis, and dysregulation of mitophagy. Mitophagy is a highly specific quality control process which eliminates dysfunctional mitochondria and promotes mitochondrial turnover, and is involved in the adaptation to nutrient stress by controlling mitochondrial mass. The dysregulation of mitochondrial turnover has both a positive and negative role in cancer. This review will begin with a basic overview of the molecular mechanisms of mitophagy, and highlight recent trends in mitophagy from cancer studies. We will conclude this review by discussing areas of research in normal mitophagy that have yet to be explored in the context of cancer such as mitochondrial proteases, the mitochondrial unfolded protein response, and mitokine action. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux.
authors.affiliation: Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea; Department of Medical Science, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea.
authors.forename: Joon Young
authors.initials: JY
authors.lastname: Chang
authors.affiliation: Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea.
authors.forename: Hyon-Seung
authors.initials: HS
authors.lastname: Yi
authors.affiliation: Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea; Department of Medical Science, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea.
authors.forename: Hyeon-Woo
authors.initials: HW
authors.lastname: Kim
authors.affiliation: Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Republic of Korea. Electronic address: minhos@cnu.ac.kr.
authors.forename: Minho
authors.initials: M
authors.lastname: Shong
mesh_terms: D000818:Animals; D029742:Caenorhabditis elegans Proteins / Q000502:physiology; D002471:Cell Transformation, Neoplastic; D018450:Disease Progression; D006801:Humans; D063154:Mitochondrial Dynamics; D024101:Mitochondrial Proteins / Q000235:genetics / Q000502:physiology; D063306:Mitophagy / Q000502:physiology; D008954:Models, Biological; D009154:Mutation; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology; D009369:Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D010447:Peptide Hydrolases / Q000502:physiology; D020033:Protein Isoforms / Q000502:physiology; D056811:Unfolded Protein Response
chemical_list: D029742:Caenorhabditis elegans Proteins; D024101:Mitochondrial Proteins; D009363:Neoplasm Proteins; D020033:Protein Isoforms; D010447:Peptide Hydrolases
keywords: Cancer; Mitochondrial unfolded protein response; Mitokine; Mitophagy