Molecular Mechanisms of MEG3 in Suppressing Malignant Progression of Nasopharyngeal Carcinoma through a Multidimensional Regulatory Network
BAO Weijing, NING Jiayu, WEI Rifu, et al
Ningde Municipal Hospital Affiliated to Ningde Normal University / Ningde Clinical Medical College, Fujian Medical University, Fujian Ningde 352100, China
摘要目的: 旨在阐明长链非编码RNA MEG3对鼻咽癌细胞恶性生物学行为(增殖、迁移、侵袭及凋亡)的调控作用,并解析其分子机制。方法: 通过体外构建鼻咽癌细胞系TW03、CNE-2的MEG3过表达模型,采用qRT-PCR检测基因表达水平,结合CCK-8法、Transwell实验及流式细胞术系统性评估MEG3对细胞增殖、迁移侵袭及凋亡的影响。结果: 相较于正常鼻咽上皮细胞NP69,鼻咽癌细胞中MEG3表达显著下调(0.45±0.03 vs 1.00±0.00,P<0.05)。过表达MEG3后,其mRNA水平升高至5.29±0.05(F=398.057,P<0.01),并显著抑制NPC细胞增殖(96h OD值:0.72±0.04 vs 1.25±0.05,F=9.543,P<0.05)、迁移(32.6±3.1 vs 156.3±8.2,F=1336.342,P<0.05)及侵袭能力(28.4±2.9 vs 142.5±7.5,F=1388.434,P<0.05),同时诱导凋亡率升高至8.09±0.11%(F=801.043,P<0.05)。结论: MEG3在鼻咽癌中呈现表达缺失特征,其功能恢复可通过靶向抑制上皮-间质转化(EMT)进程,有效遏制肿瘤细胞的恶性表型,提示MEG3可作为鼻咽癌分子靶向治疗的潜在干预靶点。
Abstract:Objective: To illustrate the regulatory role of long non-coding RNA MEG3 on malignant biological behaviors (proliferation, migration, invasion, and apoptosis) in nasopharyngeal carcinoma (NPC) cells and to analyze its molecular mechanisms. Methods: MEG3 overexpression models were constructed in NPC cell lines TW03 and CNE-1. qRT-PCR was employed to detect gene expression levels, while CCK-8 assay, Transwell experiments, and flow cytometry were utilized to systematically evaluate the effects of MEG3 on cell proliferation, migration, invasion, and apoptosis. Results: Compared with normal nasopharyngeal epithelial cells NP69, MEG3 expression was significantly downregulated in NPC cells (0.45±0.03 vs 1.00±0.00, P<0.05). Overexpression of MEG3 elevated its mRNA level to 5.29±0.05 (F=398.057, P<0.01), and markedly suppressed NPC cell proliferation (96h OD value: 0.72±0.04 vs 1.25±0.05, F=9.543, P<0.05), migration (32.6±3.1 vs 156.3±8.2, F=1336.342, P<0.05), and invasion (28.4±2.9 vs 142.5±7.5, F=1388.434, P<0.05), while inducing an increased apoptosis rate of 8.09±0.11% (F=801.043, P<0.05). Conclusion: MEG3 exhibits a loss-of-expression signature in NPC, and its functional restoration effectively restrains malignant phenotypes of tumor cells by targeting the inhibition of epithelial-mesenchymal transition (EMT), suggesting MEG3 as a potential therapeutic target for molecularly targeted therapy in NPC.
包伟晶, 宁佳羽, 魏日富, 陈莉, 李玲国, 何观文. MEG3通过多维度调控网络抑制鼻咽癌恶性进展的分子机制研究[J]. 河北医学, 2025, 31(10): 1646-1650.
BAO Weijing, NING Jiayu, WEI Rifu, et al. Molecular Mechanisms of MEG3 in Suppressing Malignant Progression of Nasopharyngeal Carcinoma through a Multidimensional Regulatory Network. HeBei Med, 2025, 31(10): 1646-1650.
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