Ovarian cancer (OC) is one of the most prevalent cancers with high fatality rate. In the present study, RTPCR showed that the mRNA level of CDKN2B-AS1 was significantly upregulated while the miR-411-3p was down regulated in OC cell lines. In addition, the Sh-CDKN2B-AS1 resulted in the suppression of cell growth, invasion, migration and promotion of apoptosis, and miR-411-3p showed reversed results. Further studies demonstrated that CDKN2B-AS1 could directly interact with miR-411-3p, and that there was an inverse correlation between miR-411-3p and CDKN2B-AS1. Moreover, the in vivo experiments further demonstrated that Sh-CDKN2B-AS1 could inhibit the tumor growth. In addition, we examined the effect of CDKN2B-AS1 and miR-411-3p on HIF1a/VEGF/P38 axis. Consequently, Sh-CDKN2B-AS1 could suppress this pathway. In summary, our study demonstrated that the CDKN2B-AS1 interacted with miR-411-3p contributing to carcinogenesis in OC. Meanwhile, Sh-CDKN2B-AS1 showed anti-cancer role by promoting apoptosis and inhibiting cell growth, invasion and migration. Collectively, CDKN2B-AS1 modulated these activities possibly though miR-411-3p/HIF1a/VEGF/P38 pathway. (C) 2019 Published by Elsevier Inc.