**4. MicroRNA dysregulation in ovarian cancer**

The most recently discovered epigenetic miRNAs represent ovarian tumors have recently become a phenomenon, and it was found to substantially up-regulate miR-199a, miR-200a, miR-200a, miR-214, and down-regulate miR-100 and, precisely, miR-100 and miR-214 to target the tumor suppressor, miR-214 was shown to PTEN and is associated with resistance to platinum [21, 22]. Let-7 miRNA family as one of the regulator of the MYCN pathway that linking to the platinum-resistant trait. It was recently discovered that miRNA let-7i was a tumor substantially down-regulated suppressor in platinum-resistant ovarian tumors, and restored let-7i gain-of-function chemoresistant ovarian cancer drug sensitivity cells, thus representing a biomarker and therapeutic candidate goal [23]. MiR-429, miR-200a, and miR-200b, respectively a single primary transcript was found to be clustered on epithelial-to-mesenchymal transition-regulated (EMT, a metastatic phenotype) ZEB1/SIP1 repressor, with negative regulation of miR-200a and miR-200b ZEB1/SIP1 and the development of a loop of double-negative feedback [24]. In another study, 27 miRNAs were substantially correlated with chemotherapy response, indicating a chemotherapy response miRNA (similar to DNA methylation) represent potential biomarkers for ovarian prognosis and diagnosis [25]. Regarding the regulation of miRNA genes, a group of six chromosomes, 19 miRNAs clustered on chromosome 19, and seven clusters were up-regulated on chromosome 14, DNMT-inhibitor decitabine inhibitor, showing that miRNAs can be controlled by DNA methylation [26]. What's more, an overall, collective tumor—MiRNAs' suppressive effect has been suggested by Drosha and Dicer down-regulation, involving two enzymes in the processing of miRNA, being significantly connected with an early stage of ovarian cancer and poor prognosis [27, 28].
