title: Mitophagy: Link to cancer development and therapy.
abstract: Mitophagy, the selective degradation of mitochondria via the autophagic pathway, is a vital mechanism of mitochondrial quality control in cells. Mitophagy is responsible for the removal of malfunctioning or damaged mitochondria, which is essential for normal cellular physiology and tissue development. Pathways involved in the regulation of mitophagy, tumorigenesis, and cell death are overlapping in many cases and may be triggered by common upstream signals, which converge at the mitochondria. The failure to properly modulate mitochondrial turnover in response to oncogenic stresses can either stimulate or suppress tumorigenesis. Thus, the analysis of crosstalk among the processes of mitophagy, cell death and tumorigenesis is important for the identification of targets responsible for the stimulation of cell death and selective elimination of cancer cells. In the present review, we analyze the mechanisms of mitophagy regulation, the pathways underlying the utilization of damaged mitochondria, and how intervention with mitophagy can affect tumor cell resistance to treatment.
authors.affiliation: Faculty of Basic Medicine, MV Lomonosov Moscow State University, 119991 Moscow, Russia.
authors.forename: Andrey V
authors.initials: AV
authors.lastname: Kulikov
authors.affiliation: Faculty of Basic Medicine, MV Lomonosov Moscow State University, 119991 Moscow, Russia.
authors.forename: Ekaterina A
authors.initials: EA
authors.lastname: Luchkina
authors.affiliation: Faculty of Basic Medicine, MV Lomonosov Moscow State University, 119991 Moscow, Russia; Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 17177 Stockholm, Sweden. Electronic address: vladimir.gogvadze@ki.se.
authors.forename: Vladimir
authors.initials: V
authors.lastname: Gogvadze
authors.affiliation: Faculty of Basic Medicine, MV Lomonosov Moscow State University, 119991 Moscow, Russia; Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 17177 Stockholm, Sweden. Electronic address: Boris.Zhivotovsky@ki.se.
authors.forename: Boris
authors.initials: B
authors.lastname: Zhivotovsky
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology; D063646:Carcinogenesis; D015687:Cell Hypoxia / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D063306:Mitophagy / Q000502:physiology*; D009369:Neoplasms / Q000209:etiology* / Q000628:therapy; D018384:Oxidative Stress
keywords: Autophagy; Cancer; Cell death; Mitochondria; Mitophagy; Therapy