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REVIEW ARTICLE
Year : 2016  |  Volume : 12  |  Issue : 2  |  Page : 498-508

SiRNA and epigenetic aberrations in ovarian cancer


1 Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2 Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran, Iran
3 Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Correspondence Address:
Hamid Reza Mirzaei
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Post Code: 14176-13151, Tehran
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.153661

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Ovarian cancer has the most noteworthy lethal rate around gynecologic malignancies, and it is also considered as the fourth most frequent cancer in the woman in world. Two most critical barriers to treatment of ovarian malignancy are absence of early diagnostic markers and advancement of drug resistance after therapy, especially in advanced stages. Various epigenetic changes have been recognized in ovarian cancer. Recent progresses in our understanding of molecular pathogenesis of ovarian malignancy have dramatically provided potential new targets for molecularly targeted therapies. In very recent years, small interfering RNA (siRNA)-mediated gene silencing has been emerging as a novel treatment modality in preclinical studies in the light of its strong gene-specific silencing. Gene suppression mediated by RNA interference (RNAi) significantly suppressed gene expression at the messenger RNA (mRNA) and protein levels. SiRNAs have therapeutic potential for ovarian cancer through various mechanisms. In this review, we not only provide an overview of siRNA designing for epigenetic silencing of genes aberrantly expressed in ovarian cancer but also we will highlight that the epigenetically silenced genes offer new targets for therapeutic approaches based on re-expression of tumor suppressor genes via demethylating and deacetylating drugs.


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