Endometrial carcinoma (EC) is the most common cancer in women worldwide, yet little is known about the underlying molecular basis of EC development. LINC01224, a novel long non‑coding (lnc)RNA, was recently identified as an oncogene in various types of cancer. However, the function and underlying mechanism of LINC01224 in EC is still unclear. A total of 50 pairs of tumor and adjacent normal tissue from patients with EC, three EC cell lines and one human normal endometrial stromal cell (ESC) line were subjected to reverse transcription‑quantitative PCR assay to evaluate the expression levels of LINC01224. Cell Counting Kit‑8, colony formation and flow cytometry assays were used to assess cell proliferation and apoptosis. Western blotting was used to measure expression levels of apoptosis‑ and proliferation‑associated proteins and AKT3 protein. A xenograft model of HEC1A cells was established to validate the in vivo function of LINC01224 in EC tumor growth. Starbase 3.0 database prediction and luciferase reporter and RNA pull‑down assays were performed to verify the binding sites between LINC01224 and microRNA (miR)‑485‑5p and miR‑485‑5p and AKT3. LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. The upregulation of LINC01224 was negatively associated with survival of patients with EC. Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells; LINC01224 directly bound to and downregulated miR‑485‑5p to elevate the expression levels of AKT3, thereby promoting EC progression. LINC01224 depletion in EC cells hindered tumor growth in a xenograft model. The tumor suppressing effect of LINC01224‑knockdown on EC progression was partly rescued by treatment with miR‑485‑5p inhibitor. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR‑485‑5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.

中文翻译：

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长链非编码RNA LINC01224通过靶向子宫内膜癌中的miR-485-5p调节AKT3表达，促进细胞增殖并抑制细胞凋亡。

子宫内膜癌 (EC) 是全球女性最常见的癌症，但对 EC 发展的潜在分子基础知之甚少。LINC01224 是一种新型长链非编码 (lnc) RNA，最近被鉴定为多种癌症的致癌基因。然而，LINC01224在EC中的功能和潜在机制尚不清楚。对来自 EC 患者、3 个 EC 细胞系和 1 个人类正常子宫内膜基质细胞 (ESC) 系的总共 50 对肿瘤和邻近正常组织进行逆转录-定量 PCR 测定，以评估 LINC01224 的表达水平。Cell Counting Kit‑8、集落形成和流式细胞术检测用于评估细胞增殖和凋亡。使用蛋白质印迹法测量细胞凋亡和增殖相关蛋白和 AKT3 蛋白的表达水平。体内LINC01224 在 EC 肿瘤生长中的功能。进行了 Starbase 3.0 数据库预测和荧光素酶报告基因和 RNA 下拉分析，以验证 LINC01224 与 microRNA (miR)-485-5p 和 miR-485-5p 和 AKT3 之间的结合位点。LINC01224 表达在 EC 肿瘤组织和细胞系中均显着上调。LINC01224 的上调与 EC 患者的存活率呈负相关。在功能上，LINC01224促进EC细胞增殖并抑制细胞凋亡；LINC01224 直接结合并下调 miR-485-5p 以提高 AKT3 的表达水平，从而促进 EC 进展。EC 细胞中的 LINC01224 耗竭阻碍了异种移植模型中的肿瘤生长。用 miR-485-5p 抑制剂治疗部分挽救了 LINC01224 敲低对 EC 进展的肿瘤抑制作用。目前的数据证明了 LINC01224 在 EC 中的表达水平、临床相关性和功能机制。LINC01224通过海绵miR-485-5p提高AKT3表达水平促进EC发育；这可能为 EC 治疗提供一个有希望的治疗靶点途径。