OBJECTIVE  To explore the phenotypic changes and possible mechanisms of lncRNA OIP5-AS1 on the proliferation, migration, apoptosis, invasion and cycle of ovarian epithelial cells IOSE80.

METHODS  The clinical data of patients were collected from TCGA database and GEO database. After R package analysis, the differential expression of OIP5-AS1 was visualized in the volcanic map. The correlation between survival rate and OIP5-AS1 was analyzed by Kaplan-Meier. The IOSE80 cell model of OIP5-AS1 over expression and silencing was constructed with lentivirus vector. The expression of OIP5-AS1 was verified by RT-qPCR. Cell proliferation was detected by CCK-8. Invasion was detected by Transwell. Cell migration was detected by scratch test. Cell cycle and apoptosis were detected by flow cytometry. Western blotting was used to detect the expression of E-cadherin and N-cadherin, as well as the expression of cyclin-dependent kinase(CDK) and cyclin-G-related kinase(GAK).

RESULTS  RT-qPCR results showed that IOSE80 cell lines over expressing and silencing OIP5-AS1 were successfully constructed. CCK-8 results showed that overexpressing OIP5-AS1 promoted the proliferation of IOSE80 cells. Scratch test results showed that overexpressing OIP5-AS1 promoted the migration of IOSE80 cells. Transwell results showed that overexpressing OIP5-AS1 would increase the invasiveness of IOSE80 cells. Flow cytometry results showed that overexpression of OIP5-AS1 weakened the apoptosis of IOSE80 cells and promoted the progress of cell cycle. Western blotting results showed that overexpression of OIP5-AS1 downregulated the expression of E-cadherin and upregulated the expression of N-cadherin, while overexpression of OIP5-AS1 increased the expression of CDK and GAK proteins.

CONCLUSION  LncRNA OIP5-AS1 further interferes with the regulation of IOSE80 cell cycle by up regulating the expression of CDK and GAK, and then indirectly regulates the malignant phenotype of ovarian epithelial cells.