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dc.contributor.authorMajidinia, M
dc.contributor.authorSadeghpour, A
dc.contributor.authorMehrzadi, S
dc.contributor.authorReiter, RJ
dc.contributor.authorKhatami, N
dc.contributor.authorYousefi, B
dc.date.accessioned2018-08-26T05:00:37Z
dc.date.available2018-08-26T05:00:37Z
dc.date.issued2017
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/38963
dc.description.abstractDNA repair is responsible for maintaining the integrity of the genome. Perturbations in the DNA repair pathways have been identified in several human cancers. Thus, compounds targeting DNA damage response (DDR) hold great promise in cancer therapy. A great deal of effort, in pursuit of new anticancer drugs, has been devoted to understanding the basic mechanisms and functions of the cellular DNA repair machinery. Melatonin, a widely produced indoleamine in all organisms, is associated with a reduced risk of cancer and has multiple regulatory roles on the different aspects of the DDR and DNA repair. Herein, we have mainly discussed how defective components in different DNA repair machineries, including homologous recombination (HR), nonhomologous end-joining (NHEJ), base excision repair (BER), nucleotide excision repair (NER), and finally DNA mismatch repair (MMR), can contribute to the risk of cancer. Melatonin biosynthesis, mode of action, and antioxidant effects are reviewed along with the means by which the indoleamine regulates DDR at the transduction, mediation, and functional levels. Finally, we summarize recent studies that illustrate how melatonin can be combined with DNA-damaging agents to improve their efficacy in cancer therapy.
dc.language.isoEnglish
dc.relation.ispartofJournal of pineal research
dc.subjectAnimals
dc.subjectCell Cycle
dc.subjectCircadian Rhythm
dc.subjectDNA
dc.subjectDNA Damage
dc.subjectDNA Repair
dc.subjectHumans
dc.subjectMelatonin
dc.subjectMice
dc.subjectNeoplasms
dc.subjectPineal Gland
dc.subjectProtective Agents
dc.subjectRats
dc.titleMelatonin: A pleiotropic molecule that modulates DNA damage response and repair pathways.
dc.typearticle
dc.citation.volume63
dc.citation.issue1
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1111/jpi.12416


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