MEG3-miR-770-5p-ARPC2 Pathway In EOC’s Disease

Epithelial ovarian cancer (EOC) incidents occultly and is usually discovered with the later classification or has been transferred. As we all know, aberrant proliferation and migration of tumor cell are closely related to this process and contribute to the occurrence and development of the disease. LncRNA-MEG3 (Maternally expressed gene 3) was known in the pathogenesis of many cancers by affecting cell migration and proliferation, almost of which expounded its function in P53 pathway or DNA methylation, while not so many evidences had demonstrated the function as the role of host gene. Recent study has clarified the function of MEG3 in EOC, but no research paid attention to its function in its downstream genetic receptors. Our group examined the miRNA expression of MEG3 in epithelial ovarian cancer and benign ovarian tumors by Quantitative RT-PCR (qRT-PCR), we found that the expression in experimental group was lower than the control group, there are significant differences. In this study, we took MEG3 as the starting point. Bioinformatics analysis revealed that the final intron surface of lncRNA-MEG3 encodes miR-770-5p which is highly conserved in evolution. So we explore the possibility that MEG3 involved in the pathogenesis of epithelial ovarian cancer as host genes by miR-770-5p.We used bioinformatics software to predict potential target gene of miR-770-5p and results showed that ARPC2 was one of them. By using quantitative RT-PCR (qRT-PCR) and western blot method, we detected the expression of ARPC2, the target gene of miR-770-5p, and found that miR-770-5p showed low expression in EOC tissues whereas ARPC2 showed high expression. We chose OMC685 and HEY cell line as our experimental Cell Lines. The ability of cell migration and proliferation was enhanced in vitro as MEG3 siRNA was transforded. Dual luciferase reporter gene assay was used to validate that miR-770-5p regulated its target gene ARPC2 by binding to the 3’untranslated region (3’UTR) of ARPC2 in vivo. After transfection of miR-770-5p inhibitor in cells to make miR-770-5p down-regulated, we found that ARPC2 showed high expression level, and the migration and proliferation ability of cells was Strengthed. By further using RNA interference technology to reduce the expression of ARPC2, migration and proliferation ability of cells were partly inhibited. Therefore, we can draw the conclusion that reduction of host gene expression of MEG3 affected the expression level of miR-770-5p, and then the target gene ARPC2 of miR-770-5p showed high expression. A series of changes led to the migration and proliferation ability inhibition of cells. They might conspire to EOC occurrence.In conclusion, this study is the first time to detect the MEG3-miR-770-5p-ARPC2 pathway in the pathogenesis of EOC and provides new clues and theoretical basis for detecting the pathogenesis of EOC.