The polycystic ovary syndrome (PCOS), a common endocrine disorder, is mainly related to infertility. Moreover, it is characterized by promoted androgen, suppressed ovulation and insulin resistance. Long non-coding RNA X inactive specific transcript (lncRNA XIST), known as an oncogene or a cancer inhabited factor, is involved in several disease. However, the diagnostic mechanisms of lncRNA XIST in PCOS have not been clarified. Our study aimed to explain whether lncRNA XIST regulates KGN cells proliferation and apoptosis via microRNA (miR)-212-3p/RASA1 axis in PCOS. Levels of lncRNA XIST, miR-212-3p and RASA1 in KGN cells were detected through reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay. Fluorescence in situ Hybridization (FISH) was performed to confirm the expression of lncRNA XIST and miR-212-3p in KGN cells. StarBase and dual-luciferase reporter assay were applied for exploring the interaction between miR-212-3p and RASA1. Cell viability, apoptosis, protein expression of Bcl-2 and Bax were assessed by MTT, flow cytometry analysis, RT-qPCR and western blot, respectively. We found that lncRNA XIST was low-expressed, miR-212-3p was over-expressed, and RASA1 was dramatically down-regulated in KGN cells. LncRNA XIST negatively regulated miR-212-3p expression in KGN cells. MiR-212-3p interacted with RASA1 and negatively regulated RASA1 levels in KGN cells. Up-regulation of lncRNA XIST signally decreased cells viability, stimulated more apoptotic cells, enhanced Bax expression, and depressed Bcl-2 level in KGN cells. However, these observations were abolished after miR-212-3p mimic treatment. Furthermore, miR-212-3p inhibitor significantly inhibited cell proliferation, enhanced more apoptotic cells, increased Bax expression, and decreased Bcl-2 level in KGN cells, and these effects were eliminated by RASA1-siRNA transfection. Our observations revealed that lncRNA XIST protects against PCOS through regulating miR-212-3p/RASA1 axis, suggesting that lncRNA XIST may be a promising therapeutic target for PCOS therapy.

多囊卵巢综合症（PCOS）是一种常见的内分泌疾病，主要与不孕有关。此外，其特点是促进雄激素、抑制排卵和胰岛素抵抗。长非编码RNA X失活特异性转录本（lncRNA XIST）被称为癌基因或癌症居住因子，与多种疾病有关。然而，lncRNA XIST在PCOS中的诊断机制尚未阐明。我们的研究旨在解释 lncRNA XIST 是否通过 microRNA (miR)-212-3p/RASA1 轴调节 PCOS 中 KGN 细胞的增殖和凋亡。通过逆转录定量聚合酶链反应（RT-qPCR）检测KGN细胞中lncRNA XIST、miR-212-3p和RASA1的水平。进行荧光原位杂交（FISH）以确认 KGN 细胞中 lncRNA XIST 和 miR-212-3p 的表达。应用 StarBase 和双荧光素酶报告基因测定来探索 miR-212-3p 和 RASA1 之间的相互作用。分别通过MTT、流式细胞术分析、RT-qPCR和蛋白质印迹评估细胞活力、凋亡、Bcl-2和Bax蛋白表达。我们发现 KGN 细胞中 lncRNA XIST 低表达，miR-212-3p 过表达，RASA1 显着下调。 LncRNA XIST 负向调节 KGN 细胞中 miR-212-3p 的表达。 MiR-212-3p 与 RASA1 相互作用并负向调节 KGN 细胞中的 RASA1 水平。 lncRNA XIST 的上调显着降低了 KGN 细胞中的细胞活力、刺激更多的细胞凋亡、增强了 Bax 表达并降低了 Bcl-2 水平。然而，这些观察结果在 miR-212-3p 模拟物治疗后被废除。此外，miR-212-3p抑制剂显着抑制KGN细胞中的细胞增殖，增强更多的细胞凋亡，增加Bax表达，降低Bcl-2水平，而这些影响可通过RASA1-siRNA转染消除。我们的观察结果表明，lncRNA XIST 通过调节 miR-212-3p/RASA1 轴来预防 PCOS，这表明 lncRNA XIST 可能是 PCOS 治疗的一个有前景的治疗靶点。