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Metformin: Prevention of Genomic Instability and Cancer: A Review Publisher Pubmed



Najafi M1 ; Cheki M2 ; Rezapoor S3 ; Geraily G4 ; Motevaseli E5 ; Carnovale C6 ; Clementi E7, 8 ; Shirazi A4
Authors
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Authors Affiliations
  1. 1. Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Science, Kermanshah, Iran
  2. 2. Department of Radiologic Technology, Faculty of Paramedicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  3. 3. Department of Radiology, Faculty of Paramedical, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Medical Physics and Biomedical Engineering, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Biomedical and Clinical Sciences L. Sacco, Unit of Clinical Pharmacology, ASST Fatebenefratelli-Sacco University Hospital, Universita di Milano, Milan, Italy
  7. 7. Scientific Institute, IRCCS E. Medea, Bosisio Parini, Lecco, Italy
  8. 8. Unit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences, Consiglio Nazionale delle Ricerche Institute of Neuroscience, L. Sacco University Hospital, Universita di Milano, Milan, Italy

Source: Mutation Research - Genetic Toxicology and Environmental Mutagenesis Published:2018


Abstract

The diabetes drug metformin can mitigate the genotoxic effects of cytotoxic agents and has been proposed to prevent or even cure certain cancers. Metformin reduces DNA damage by mechanisms that are only incompletely understood. Metformin scavenges free radicals, including reactive oxygen species and nitric oxide, which are produced by genotoxicants such as ionizing or non-ionizing radiation, heavy metals, and chemotherapeutic agents. The drug may also increase the activities of antioxidant enzymes and inhibit NADPH oxidase, cyclooxygenase-2, and inducible nitric oxide synthase, thereby limiting macrophage recruitment and inflammatory responses. Metformin stimulates the DNA damage response (DDR) in the homologous end-joining, homologous recombination, and nucleotide excision repair pathways. This review focuses on the protective properties of metformin against genomic instability. © 2018 Elsevier B.V.
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