卵巢癌（OC）已成为全世界女性致命的妇科恶性肿瘤。靶向治疗对于 OC 患者来说是一种有前途的治疗选择，识别生物标志物并探索分子机制是必要的。本研究探讨了长链非编码RNA瞬时受体电位通道亚家族M成员2反义RNA（TRPM2-AS）在OC中的功能和机制。利用逆转录定量聚合酶链反应 (RT-qPCR) 分析 OC 细胞中的 TRPM2-AS 表达。采用细胞计数试剂盒-8 (CCK-8) 和集落形成实验来探讨 TRPM2-AS 对 OC 细胞活力和增殖的影响。使用 TdT 介导的 dUTP Nick-End 标记 (TUNEL) 和流式细胞术分析检测细胞凋亡。对细胞凋亡标记物的蛋白质表达进行蛋白质印迹分析。应用 RNA Pulldown 或荧光素酶报告基因测定来探索 TRPM2-AS 和 miR-6764-5p 之间的相互作用或 miR-6764-5p 和 TRPM2 的结合。结果显示TRPM2-AS在OC细胞中高表达且主要定位于细胞质。 TRPM2-AS 耗竭抑制 OC 细胞活力和增殖，同时增加细胞凋亡率。 TRPM2 在 OC 细胞中表现出高水平，并受到 TRPM2-AS 的正向调节。 TRPM2-AS 与 miR-6764-5p 相互作用，从而上调 TRPM2 表达。此外，TRPM2 过表达逆转了 TRPM2-AS 耗竭对恶性 OC 细胞过程的抑制作用。总之，TRPM2-AS 通过与 miR-6764-5p 相互作用调节 TRPM2 水平，促进 OC 细胞活力和增殖，同时增强细胞凋亡。© 2024。作者。

Ovarian cancer (OC) becomes a fatal gynecologic malignant cancer in females worldwide. Target therapy is a promising therapeutical choice for patients with OC, and identifying biomarkers and exploring molecular mechanisms are necessary. In this study, the functions and mechanism of long noncoding RNA transient receptor potential cation channel subfamily M member 2 antisense RNA (TRPM2-AS) in OC were explored. TRPM2-AS expression in OC cells was analyzed utilizing reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8) and colony forming assays were carried out to explore the influence of TRPM2-AS on OC cell viability and proliferation. Cell apoptosis was detected using TdT-mediated dUTP Nick-End labeling (TUNEL) and flow cytometry analysis. Protein expression of apoptotic markers was subjected to western blotting. RNA pulldown or luciferase reporter assays were applied to explore the interaction between TRPM2-AS and miR-6764-5p or the binding of miR-6764-5p and TRPM2. The results showed that TRPM2-AS is highly expressed in OC cells and was mainly localized in cytoplasm. TRPM2-AS depletion suppressed OC cell viability and proliferation while increasing cell apoptotic rate. TRPM2 displayed a high level in OC cells and was positively regulated by TRPM2-AS. TRPM2-AS interacted with miR-6764-5p and thereby upregulated TRPM2 expression. In addition, TRPM2 overexpression reversed the repressive impact of TRPM2-AS depletion on malignant OC cellular process. In conclusion, TRPM2-AS promotes OC cell viability and proliferation while enhancing cell apoptosis through interaction with miR-6764-5p to regulate TRPM2 level.© 2024. The Author(s).