As one of the most common cancers in female, ovarian cancer (OC) has become a serious public burden now. Mounting researches have indicated long noncoding RNAs (lncRNAs) can affect many biological processes including cancer development. LncRNA LBX2-AS1 was identified to be an oncogene in some cancers, but the role of LBX2-AS1 in OC remains to be elucidated. Bioinformatics analysis and experiments including ChIP, RT-qPCR, RIP, luciferase reporter, western blot and CCK-8 were performed to explore the role of LBX2-AS1 in OC. LBX2-AS1 expression was markedly increased in OC tissues and cell lines. Functionally, LBX2-AS1 silencing inhibited cell proliferation, migration and stemness but facilitated cell apoptosis in OC. Moreover, depletion of LBX2-AS1 suppressed tumor growth of OC in vivo. Mechanically, LBX2-AS1 was activated by transcriptional factor ELK1. ELK1 enhanced the expression of LBX2-AS1 in OC cells. In addition, miR-4784 was confirmed to be sponged by LBX2-AS1. There was a negative expression correlation between LBX2-AS1 and miR-4784 in OC tissues. Subsequently, KDM5C was identified to be a direct target of miR-4784 in OC cells. KDM5C was negatively regulated by miR-4784 and positively regulated by LBX2-AS1 in terms of expression level. Upregulation of KDM5C reversed the inhibitory effect of LBX2-AS1 depletion on the progression of OC. This study proved that ELK1 activated-LBX2-AS1 aggravated the progression of OC by targeting the miR-4784/KDM5C axis, suggesting that LBX2-AS2 may be a promising diagnostic biomarker of OC.

卵巢癌（OC）作为女性最常见的癌症之一，现已成为严重的公众负担。越来越多的研究表明长链非编码 RNA (lncRNA) 可以影响许多生物过程，包括癌症的发展。 LncRNA LBX2-AS1 被确定为某些癌症中的癌基因，但 LBX2-AS1 在 OC 中的作用仍有待阐明。通过生物信息学分析和实验（包括 ChIP、RT-qPCR、RIP、荧光素酶报告基因、蛋白质印迹和 CCK-8）来探讨 LBX2-AS1 在 OC 中的作用。 LBX2-AS1 表达在 OC 组织和细胞系中显着增加。从功能上讲，LBX2-AS1 沉默可抑制 OC 中的细胞增殖、迁移和干性，但促进细胞凋亡。此外，LBX2-AS1的消耗抑制了体内OC的肿瘤生长。机械上，LBX2-AS1 被转录因子 ELK1 激活。 ELK1 增强 OC 细胞中 LBX2-AS1 的表达。此外，miR-4784被证实被LBX2-AS1吸收。 OC组织中LBX2-AS1和miR-4784之间存在负表达相关性。随后，KDM5C 被确定为 OC 细胞中 miR-4784 的直接靶标。 KDM5C的表达水平受miR-4784负向调节，并受LBX2-AS1正向调节。 KDM5C 的上调逆转了 LBX2-AS1 缺失对 OC 进展的抑制作用。这项研究证明，ELK1 激活的 LBX2-AS1 通过靶向 miR-4784/KDM5C 轴，加剧了 OC 的进展，表明 LBX2-AS2 可能是一种有前途的 OC 诊断生物标志物。