河北医科大学学报 ›› 2025, Vol. 46 ›› Issue (8): 881-889.doi: 10.3969/j.issn.1007-3205.2025.08.003

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miR-106a-5p对鼻咽癌细胞增殖、迁移和侵袭能力的影响

  

  1. 1.河北省唐山市人民医院耳鼻咽喉科,河北 唐山 063000;2.华北理工大学研究生院,河北 唐山 063000;3.河北省唐山市人民医院中心实验室,河北省分子肿瘤重点实验室,河北 唐山 063000

  • 出版日期:2025-08-25 发布日期:2025-08-29
  • 作者简介:张立杰(1975-),女,河北唐山人,河北省唐山市人民医院副主任医师,医学学士,从事耳鼻咽喉头颈外科研究。

  • 基金资助:
    河北省分子肿瘤学重点实验室项目(SZX2020043)

Effects of miR-106a-5p on proliferation, migration and invasion of nasopharyngeal carcinoma cells

  1. 1.Department of Otolaryngology, People′s Hospital of Tangshan City, Hebei Province, Tangshan 
    063000, China; 2.Graduate School, North China University of Science and Technology, 
    Hebei Province, Tangshan 063000, China; 3.Department of Central Laboratory,
    People′s Hospital of Tangshan City, Key Laboratory of Molecular 
    Oncology of Hebei Province, Tangshan 063000, China

  • Online:2025-08-25 Published:2025-08-29

摘要: 目的 探讨miR-106a-5p/程序性死亡配体1(programmed death-ligand 1,PD-L1)轴对鼻咽癌(nasopharyngeal carcinoma,NPC)细胞恶性生物学行为的影响及分子机制。
方法 通过实时荧光定量PCR检测NPC细胞系HNE1及永生化正常鼻咽上皮细胞NP69中miR-106a-5p和PD-L1 mRNA的表达水平;Western blot检测PD-L1蛋白表达;双荧光素酶报告实验验证miR-106a-5p与PD-L1之间的靶向调控关系;miR-106a-5p mimics及inhibitor、si-PD-L1及PD-L1转染HNE1细胞;细胞计数试剂盒8检测细胞增殖能力;划痕实验和Transwell实验检测细胞迁移和侵袭能力。
结果 NPC细胞中miR-106a-5p和PD-L1的表达水平显著高于正常鼻咽上皮细胞(miR-106a-5p:P=0.001,PD-L1-mRNA:P=0.012,PD-L1-蛋白:P=0.008)。双荧光素酶报告实验表明PD-L1是miR-106a-5p的直接靶点。miR-106a-5p mimics显著上调PD-L1的mRNA和蛋白水平(P=0.010; P=0.037),而miR-106a-5p inhibitor显著抑制PD-L1的表达(P<0.001)。PD-L1过表达导致miR-106a-5p水平显著升高(P<0.05),敲低PD-L1导致miR-106a-5p水平显著降低(P<0.05)。过表达miR-106a-5p或PD-L1均可显著增强HNE1细胞增殖、侵袭和迁移能力(均P<0.05),同时敲低PD-L1或miR-106a-5p均可逆转这一效应(均P<0.05)。相反,敲低miR-106a-5p或PD-L1均显著抑制细胞增殖、侵袭和迁移能力,同时过表达PD-L1或miR-106a-5p能够逆转该抑制作用(均P<0.05)。
结论 miR-106a-5p与PD-L1间存在正反馈调控,促进NPC细胞的增殖、迁移和侵袭。


关键词: 鼻咽癌, 细胞增殖, 迁移和侵袭

Abstract: Objective To investigate the impact of the miR-106a-5p/programmed death-ligand 1 (PD-L1) axis on the malignant biological behavior of nasopharyngeal carcinoma (NPC) cells and its molecular mechanism. 
Methods The expression levels of miR-106a-5p and PD-L1 mRNA in the NPC cell line HNE1 and immortalized normal nasopharyngeal epithelial cell line NP69 were measured using quantitative real-time PCR (RT-qPCR), and PD-L1 protein expression was assessed by Western blotting. A dual-luciferase reporter assay was performed to verify the direct regulatory relationship between miR-106a-5p and PD-L1. HNE1 cells were transfected with miR-106a-5p mimics, inhibitors, si-PD-L1, or PD-L1 overexpression plasmids. Cell proliferation was evaluated by the CCK-8 assay, while cell migration and invasion were assessed using scratch assays and Transwell assays, respectively. 
Results The expression levels of miR-106a-5p and PD-L1 were significantly higher in NPC cells than in normal nasopharyngeal epithelial cells (miR-106a-5p: P=0.001,PD-L1-mRNA: P=0.012, PD-L1-protein: P=0.008). The dual-luciferase reporter assay confirmed that PD-L1 was a direct target of miR-106a-5p. miR-106a-5p significantly increased the mRNA and protein levels of PD-L1 (P=0.010; P=0.037), whereas the miR-106a-5p inhibitor markedly suppressed PD-L1 expression (P<0.001). Overexpression of PD-L1 led to a significant upregulation of miR-106a-5p (P<0.05), and knockdown of PD-L1 significantly reduced miR-106a-5p levels (P<0.05). Overexpression of either miR-106a-5p or PD-L1 significantly enhanced the proliferation, invasion and migration of HNE1 cells (bothP<0.05), while knockdown of either PD-L1 or miR-106a-5p reversed these effects (both P<0.05). Conversely, knockdown of miR-106a-5p or PD-L1 significantly inhibited cell proliferation, invasion and migration, and overexpression of either PD-L1 or miR-106a-5p could reverse this inhibition (both P<0.05). 
Conclusion There is a positive feedback regulation between miR-106a-5p and PD-L1, which promotes the proliferation, migration, and invasion of NPC cells.


Key words: nasopharyngeal carcinoma, cell proliferation, migration and invasion