Chen Yanxia, Wang Jing, Heng Youqiang, Guo Yu, Ding Ka, Ma Cailing
Department of Gynecology, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Sci Rep. 2025 Jul 1;15(1):20541. doi: 10.1038/s41598-025-08727-3.
Long non-coding RNA (lncRNA) exhibits a crucial role in multiple human malignancies. The expression of lncRNA MIR155HG, reportedly, is aberrantly up-regulated in several types of tumors. In this research, we studied the role and mechanism of MIR155HG in the progression of cervical cancer (CC). We analyzed the expression pattern of MIR155HG in CC patients using public database TCGA, and overexpressed its expression in HeLa cells to explore its cellular functions. Cellular phenotype experiments were conducted to assess the influence of MIR155HG on HeLa cells, including proliferation, cell cycle, migration, invasion, and cisplatin sensitivity. Then we evaluated the impact on epithelial-mesenchymal transition (EMT) of MIR155HG and identified the underlying regulatory mechanism. We found that MIR155HG was highly expressed and positively correlated with overall survival (OS) prognosis results in CC patients. Overexpression of MIR155HG (MIR155HG-OE) demonstrated higher proliferation and migration levels in HeLa cells, while MIR155HG inhibited the apoptosis rate of HeLa cells. Meanwhile, we found MIR155HG can reduce the effect of cisplatin sensitivity on HeLa cells. Besides this, MIR155HG-OE significantly changed the expression pattern of EMT biomarkers, including ZEB1, TWIST1, Vimentin, N-cadherin, and E-cadherin. To explore the underlying mechanism, we found MIR155HG can promote ZEB1 expression by sponging miR-409-3p, forming a competitive endogenous RNA system to inhibit cisplatin sensitivity. In this study, we deeply explored the molecular and cellular functions of MIR155HG in CC cells. Our results highlight the important role and potential targeting value of MIR155HG in CC pathogenesis and development.
长链非编码RNA（lncRNA）在多种人类恶性肿瘤中发挥着关键作用。据报道，lncRNA MIR155HG的表达在几种类型的肿瘤中异常上调。在本研究中，我们探讨了MIR155HG在宫颈癌（CC）进展中的作用及机制。我们使用公共数据库TCGA分析了CC患者中MIR155HG的表达模式，并在HeLa细胞中过表达其表达以探索其细胞功能。进行细胞表型实验以评估MIR155HG对HeLa细胞的影响，包括增殖、细胞周期、迁移、侵袭和顺铂敏感性。然后我们评估了MIR155HG对上皮-间质转化（EMT）的影响，并确定了潜在的调控机制。我们发现MIR155HG在CC患者中高表达，且与总生存（OS）预后结果呈正相关。MIR155HG过表达（MIR155HG-OE）在HeLa细胞中表现出更高的增殖和迁移水平，而MIR155HG抑制了HeLa细胞的凋亡率。同时，我们发现MIR155HG可降低顺铂对HeLa细胞敏感性的影响。除此之外，MIR155HG-OE显著改变了EMT生物标志物的表达模式，包括ZEB1、TWIST1、波形蛋白、N-钙黏蛋白和E-钙黏蛋白。为探索潜在机制，我们发现MIR155HG可通过海绵吸附miR-409-3p促进ZEB1表达，形成竞争性内源性RNA系统以抑制顺铂敏感性。在本研究中，我们深入探讨了MIR155HG在CC细胞中的分子和细胞功能。我们的结果突出了MIR155HG在CC发病机制和发展中的重要作用及潜在靶向价值。
