Long non-coding RNA CCAT2 regulates proliferation, drug sensitivity and metastasis of ovarian cancer

Abstract

IntroductionReports suggest that lncRNAs have implications in the development of several diseases including cancer. It is therefore believed that lncRNAs may act as therapeutic targets for cancer treatment. The treatment of ovarian cancer is mainly obstructed by lack of biomarkers and efficient drug targets. Against this backdrop, this study was undertaken to reveal the role and therapeutic implications of lncRNA CCAT2 in ovarian cancer.Material and methodsExpression analysis was carried out with quantitative real-time polymerase chain reaction (qRT-PCR). Transfections were carried out using Lipofectamine 2000 reagent. Cell counting kit 8 (CCK-8) assays were used to determine the cell viability. AO/EB and annexin V/propidium iodide (PI) were used for detection of apoptosis. Wound healing and transwell assays were used to determine cell migration and invasion. The expression of the proteins was estimated by western blotting.ResultsThe results showed that the expression of CCAT2 was significantly overexpressed in ovarian cancer tissues and cell lines. Si-RNA mediated silencing of CCAT2 resulted in the decrease of proliferation rate and colony formation potential of the OVACAR-3 cells via induction of apoptotic cell death, which was also accompanied by cleavage of PARP, downregulation of Bcl-2 and upregulation of Bax, caspase-3 and caspase-9. Suppression of CCAT2 enhanced the chemosensitivity of the OVACAR-3 cells to cisplatin and also decreased their migration and invasion.ConclusionsThe findings of this study revealed that lncRNA CCAT2 suppression inhibits the proliferation, drug sensitivity, and metastasis of ovarian cancer and may prove beneficial in ovarian cancer management.