宫颈癌（CC）是影响女性生殖系统最常见的恶性肿瘤之一。尽管如此，目前的 CC 治疗方法仍存在各种缺点。因此，寻求新的干预目标具有重要意义。研究表明，长非编码RNA（lncRNA）长基因间非蛋白编码RNA 2487（LINC02487）可以抑制口腔鳞状细胞癌（OSCC）的发展。然而，其在CC中的功能和潜在机制仍不清楚，因此，本研究旨在研究LINC02487在CC中的作用和潜在机制。使用实时定量聚合酶链反应评估LINC02487和磷酸酶和张力蛋白同源物（PTEN）的表达。 RT-qPCR）在 CC 组织样本中进行检测并构建细胞模型。 LINC02487 被敲低或过表达，PTEN 通过转染技术在 CC (SiHa) 细胞系中被敲低。在各种处理后，使用 RT-qPCR 检查 SiHa 细胞系中 LINC02487 和 PTEN 的表达水平。通过细胞计数试剂盒（CCK）-8和集落形成测定测定细胞增殖能力，同时通过Transwell实验评估细胞侵袭和迁移能力。采用Western blot分析检测PTEN/Akt/雷帕霉素机械靶标（mTOR）信号通路中关键蛋白的水平。LINC02487和PTEN之间观察到正相关，两者均在CC细胞中表达下调和组织（p < 0.05）。体外实验表明，LINC02487 的过表达显着抑制 SiHa 细胞的集落形成 (p < 0.01)、侵袭 (p < 0.01)、迁移 (p < 0.01) 和增殖 (p < 0.01)。此外，LINC02487 过表达导致 PTEN 表达上调 (p < 0.01) 和 Akt/mTOR 信号通路抑制 (p < 0.01)，而 LINC02487 的敲低则产生相反的效果 (p < 0.01)。此外，敲除 PTEN 可以抵消 LINC02487 过表达对 CC 进展 (p < 0.01) 和 Akt/mTOR 信号通路 (p < 0.01) 的抑制作用。体外研究结果表明，LINC02487 可能通过抑制 Akt/mTOR 信号通路来阻碍 CC 的进展。 mTOR信号通路通过上调PTEN表达。因此，LINC02487有望成为治疗CC的潜在治疗靶点。

Cervical cancer (CC) ranks among the most prevalent malignant tumors affecting the female reproductive system. Nonetheless, various shortcomings exist within current treatment approaches for CC. Therefore, the quest for new intervention targets holds significant importance. Research has demonstrated that long non-coding RNA (lncRNA) long intergenic non-protein coding RNA 2487 (LINC02487) can suppress the development of oral squamous cell carcinoma (OSCC). However, its function and potential mechanisms in CC remain unclear, therefore, this study aims to investigate the role and potential mechanism of LINC02487 in CC.LINC02487 and phosphatase and tensin homolog (PTEN) expression were assessed using real-time quantitative polymerase chain reaction (RT-qPCR) in CC tissue samples and constructed cell models. LINC02487 was either knocked down or overexpressed, and PTEN was knocked down in the CC (SiHa) cell line via transfection technology. The expression levels of LINC02487 and PTEN in SiHa cell lines were examined using RT-qPCR after various treatments. Cell proliferation ability was determined through Cell Counting Kit (CCK)-8 and colony formation assays, while the ability to invade and migrate was assessed via Transwell experiments. Western blot analysis was employed to measure the levels of key proteins in the PTEN/Akt/mechanistic target of the rapamycin (mTOR) signaling pathway.A positive correlation was observed between LINC02487 and PTEN, both of which were found to be downregulated in CC cells and tissues (p < 0.05). In vitro experiments demonstrated that overexpression of LINC02487 significantly inhibited colony formation (p < 0.01), invasion (p < 0.01), migration (p < 0.01), and proliferation (p < 0.01) of SiHa cells. Furthermore, LINC02487 overexpression led to upregulation of PTEN expression (p < 0.01) and inhibition of the Akt/mTOR signaling pathway (p < 0.01), while knockdown of LINC02487 produced the opposite effect (p < 0.01). Additionally, knocking down PTEN counteracted the inhibitory effects of LINC02487 overexpression on CC progression (p < 0.01) and the Akt/mTOR signaling pathway (p < 0.01).In vitro findings suggest that LINC02487 may impede the progression of CC by suppressing the Akt/mTOR signaling pathway through the upregulation of PTEN expression. Consequently, LINC02487 holds promise as a potential therapeutic target for the treatment of CC.