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SIRT1 and gynecological malignancies

Sirtuin 1 (SIRT1), a member of the sirtuin protein family, is a nicotinamide adenine dinucleotide (NAD(+))-dependent type III histone deacetylase and mono-ADP-ribosyltransferase. SIRT1 can deacetylate histones (H1, H3, and H4) and non-histone proteins, and it is widely involved in various physiologi...

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Detalles Bibliográficos
Autores principales: Chen, Jiayu, Chen, Houzao, Pan, Lingya
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7934219/
https://www.ncbi.nlm.nih.gov/pubmed/33649834
http://dx.doi.org/10.3892/or.2021.7994
Descripción
Sumario:Sirtuin 1 (SIRT1), a member of the sirtuin protein family, is a nicotinamide adenine dinucleotide (NAD(+))-dependent type III histone deacetylase and mono-ADP-ribosyltransferase. SIRT1 can deacetylate histones (H1, H3, and H4) and non-histone proteins, and it is widely involved in various physiological and pathological processes in the body, including metabolism, aging, transcription, DNA damage and repair, apoptosis, cell cycle regulation, inflammation and cancer. Research has shown that SIRT1 is involved in tumorigenesis, tumor metastasis and chemotherapy resistance, but it exerts opposing effects and plays different roles in different pathogenic processes. Recent studies have demonstrated that SIRT1 may be implicated in the pathogenesis, development, treatment and prognosis of tumors; however, its role in gynecological tumors remains elusive. The aim of the present review was to summarize the pathogenic roles of SIRT1 in cancer, and to provide what is, to the best of our knowledge, the first review of recent advances involving SIRT1 in cervical cancer, endometrial cancer (EC) and ovarian cancer (OC). In addition, the critical research gaps regarding SIRT1, particularly its potential involvement in the concurrence of EC and cervical cancer and its antagonistic effect against poly(ADP-ribose) polymerase inhibitors in OC, were highlighted.