The aim of this study was to elucidate the role of long non-coding RNA (lncRNA) CDKN2BAS in aggravating the progression of ovarian cancer via binding growth arrest-specific 6 (GAS6).
The relative levels of CDKN2BAS and GAS6 in ovarian cancer and normal ovarian tissues were detected. In addition, their levels in ovarian cancer cases with different FIGO stages and pathological grades were detected. Pearson correlation test was applied for assessing the correlation between CDKN2BAS and GAS6 levels in ovarian cancer tissues. The roles of CDKN2BAS and GAS6 in mediating proliferative and migratory potentials in HEY and SKOV-3 cells were examined by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. Subcellular distribution of CDKN2BAS was explored. CDKN2BAS-GAS6 interaction was evaluated by RIP (RNA immunoprecipitation) assay.
CDKN2BAS was upregulated in ovarian cancer tissues, especially those with advanced FIGO stage and high pathological grade. It displayed diagnostic potential in ovarian cancer. CDKN2BAS level was positively correlated to that of GAS6 in ovarian cancer tissues. It was mainly expressed in the cytoplasm and could be interacted with GAS6. The overexpression of CDKN2BAS enhanced proliferative and migratory potentials in HEY and SKOV-3 cells. The knockdown of GAS6 partially abolished the regulatory effects of CDKN2BAS on promoting proliferative and migratory potentials in ovarian cancer.
LncRNA CDKN2BAS is upregulated in ovarian cancer. By positively interacting with GAS6, CDKN2BAS triggers the progression of ovarian cancer.