Ovarian cancer is a common gynecological malignant tumor with a high mortality rate and poor prognosis. There is inadequate knowledge of the molecular mechanisms underlying ovarian cancer. We examined the expression of methyltransferase-like 3 (METTL3) in tumor specimens using RT-qPCR, immunohistochemistry, and Western blot analysis, and tested the methylation of METTL3 by MSP. Levels of METTL3, miR-1246, pri-miR-1246 and CCNG2 were then analyzed and their effects on cell biological processes were also investigated, using in vivo assay to validate the in vitro findings. METTL3 showed hypomethylation and high expression in ovarian cancer tissues and cells. Hypomethylation of METTL3 was pronounced in ovarian cancer samples, which was negatively associated with patient survival. Decreased METTL3 inhibited the proliferation and migration of ovarian cancer cells and promoted apoptosis, while METTL3 overexpression exerted opposite effects. Mechanistically, METTL3 aggravated ovarian cancer by targeting miR-1246, while miR-1246 targeted and inhibited CCNG2 expression. High expression of METTL3 downregulated CCNG2, promoted the metabolism and growth of transplanted tumors in nude mice, and inhibited apoptosis. The current study highlights the promoting role of METTL3 in the development of ovarian cancer, and presents new targets for its treatment.

卵巢癌是常见的妇科恶性肿瘤，死亡率高，预后差。对卵巢癌的分子机制了解不足。我们使用 RT-qPCR、免疫组织化学和蛋白质印迹分析检测了肿瘤标本中甲基转移酶样 3 (METTL3) 的表达，并通过 MSP 测试了 METTL3 的甲基化。然后分析 METTL3、miR-1246、pri-miR-1246 和 CCNG2 的水平，并研究它们对细胞生物学过程的影响，使用体内测定来验证体外研究结果。 METTL3在卵巢癌组织和细胞中表现出低甲基化和高表达。 METTL3 的低甲基化在卵巢癌样本中很明显，这与患者的生存呈负相关。 METTL3的减少抑制卵巢癌细胞的增殖和迁移并促进细胞凋亡，而METTL3的过表达则产生相反的作用。从机制上讲，METTL3通过靶向miR-1246加重卵巢癌，而miR-1246靶向并抑制CCNG2表达。 METTL3的高表达下调CCNG2，促进裸鼠移植瘤的代谢和生长，抑制细胞凋亡。目前的研究强调了METTL3在卵巢癌发生发展中的促进作用，并为其治疗提出了新的靶点。