The role of long non‐coding RNAs (lncRNAs) in tumorigenesis and development of ovarian cancer (OC) has caught the attention of scientists. UNC5B antisense RNA 1 (UNC5B‐AS1) is a newly identified carcinogenic lncRNA in thyroid papillary carcinoma, but its role in OC remains unclear. This study is proposed to investigate the function and mechanism of UNC5B‐AS1 in OC. UNC5B‐AS1 expression in OC samples was obtained from gene expression profiling interactive analysis (GEPIA) based on The Cancer Genome Atlas data. Gene expressions were detected by quantitative real‐time polymerase chain reaction (RT‐qPCR) and western blot. Biological functions of UNC5B‐AS1 were assessed by cell counting kit‐8, colony formation, and caspase‐3 analysis. GEPIA revealed the UNC5B‐AS1 upregulation in OC samples. RT‐qPCR assay confirmed the upregulation of UNC5B‐AS1 in OC cells. Functionally, depletion of UCN5B‐AS1 hindered proliferation and prompted apoptosis in OC cells. Mechanistically, we found that UNC5B‐AS1 interacted with zeste 2 polycomb repressive complex 2 subunit (EZH2) to trigger trimethylation of histone H3 at lysine 27 (H3K27me3) on N‐myc downstream regulated gene‐2 (NDRG2) promoter and epigenetically repressed NDRG2. Rescue assay indicated the participation of NDRG2 in the regulation of UNC5B‐AS1 on OC progression. Together, we first illustrated that UNC5B‐AS1 promoted OC progression by regulating the H3K27me on NDRG2 via EZH2, indicating UNC5B‐AS1 as a potential molecular target for OC treatment.

中文翻译：

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UNC5B‐AS1通过EZH2调节NDRG2的H3K27me促进卵巢癌进展

长非编码RNA（lncRNA）在卵巢癌（OC）的发生和发展中的作用引起了科学家的注意。UNC5B反义RNA 1（UNC5B-AS1）是一种新发现的在甲状腺乳头状癌中致癌的lncRNA，但其在OC中的作用仍不清楚。本研究旨在探讨UNC5B‐AS1在OC中的功能和机制。OC样品中的UNC5B-AS1表达是根据癌症基因组图谱数据从基因表达谱交互分析（GEPIA）获得的。通过定量实时聚合酶链反应（RT-qPCR）和Western blot检测基因表达。UNC5B‐AS1的生物学功能通过细胞计数试剂盒‐8，集落形成和caspase-3分析进行评估。GEPIA显示OC样品中的UNC5B-AS1上调。RT-qPCR分析证实了OC细胞中UNC5B-AS1的上调。从功能上讲，UCN5B-AS1的消耗会阻止增殖并促使OC细胞凋亡。从机理上讲，我们发现UNC5B-AS1与zeste 2聚梳抑制复合物2亚基（EZH2）相互作用，触发N-myc下游调控基因2（NDRG2）启动子上赖氨酸27（H3K27me3）上组蛋白H3的三甲基化，并通过表观遗传抑制NDRG2。救援测定表明NDRG2参与了OC5B-AS1对OC进展的调节。在一起，我们首先说明UNC5B‐AS1通过EZH2调节NDRG2上的H3K27me，从而促进了OC进展，表明UNC5B‐AS1是OC治疗的潜在分子靶标。我们发现UNC5B‐AS1与zeste 2聚梳抑制复合物2亚基（EZH2）相互作用，触发N‐myc下游调控基因2（NDRG2）启动子上赖氨酸27（H3K27me3）上组蛋白H3的三甲基化，并通过表观遗传抑制NDRG2。救援测定表明NDRG2参与了OC5B-AS1对OC进展的调节。在一起，我们首先说明UNC5B‐AS1通过EZH2调节NDRG2上的H3K27me，从而促进了OC进展，表明UNC5B‐AS1是OC治疗的潜在分子靶标。我们发现UNC5B‐AS1与zeste 2聚梳抑制复合物2亚基（EZH2）相互作用，触发N‐myc下游调控基因2（NDRG2）启动子上赖氨酸27（H3K27me3）上组蛋白H3的三甲基化，并通过表观遗传抑制NDRG2。救援测定表明NDRG2参与了OC5B-AS1对OC进展的调节。在一起，我们首先说明UNC5B‐AS1通过EZH2调节NDRG2上的H3K27me，从而促进了OC进展，表明UNC5B‐AS1是OC治疗的潜在分子靶标。