Treatment Of Ovarian Cancer By MiR-98and Its Effects On Gene Expression Of KLK10

ObjectiveTo explore new therapeutic target and provide experimental evidence for treating ovarian cancer, proliferation inhibition, apoptosis, and the effects on KLK10gene expression in ovarian cancer cells induced by transfection of pre-hsa-miR98were observed.MethodsPre-hsa-miR98plasmid was constructed and transfetted into ovarian cancer cells by using lipofectamine2000. The cells were divided into control group, HmiR group, and CmiR group. Because of the plasmid with eGFP, fluorescence microscopy and flow cytometry were used to determine transfection efficiency. MTT assay and cell count growth curve were used to detect proliferation inhibition of the cells. Flow cytometry and Hoechst33258staining were used to detect the apoptosis induced by the treatment. KLK10mRNA expression was detected by RT-PCR, and KLK10protein expression was detected by ELIS A assay.ResultsThe rates of the cells transfected after24h and48h were60%in the three cell lines. After transfection, the rates of cell proliferation inhibition were increased with increase of the hours after transfection, by MTT assay. The cell growth inhibition reached the peak at72h or96h after the treatment, and the inhibition thereafter did not significantly increased with the increase of the hours, tested by cell account. Apoptosis was significantly induced by the pre-has-miR-98transfection detected by flow cytometry and Hoechst33258staining. After pre-has-miR-98transfection, KLK10mRNA levels identified by RT-PCR increased significantly, while the protein measured by ELIS A remained at a low level.Conclusion 1. Transfection of pre-has-miR-98inhibits cell proliferation in ovarian cancer cells.2. Transfection of pre-has-miR-98significantly induces cell apoptosis in ovarian cancer cells.3. After transfection of pre-has-miR-98, KLK10mRNA increased significantly, and protein levels did not increase significantly.