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miR-34a通过靶向FOXM1对鼻咽癌细胞增殖和上皮间质转化的影响
引用本文:葛思辰,蒋成义. miR-34a通过靶向FOXM1对鼻咽癌细胞增殖和上皮间质转化的影响[J]. 中华全科医学, 2021, 19(12): 2012. DOI: 10.16766/j.cnki.issn.1674-4152.002223
作者姓名:葛思辰  蒋成义
作者单位:蚌埠医学院第一附属医院耳鼻咽喉头颈外科,安徽 蚌埠 233004
基金项目:安徽省教育厅重点项目KJ20180996
摘    要:  目的  研究miR-34a通过靶向FOXM1对鼻咽癌细胞增殖、侵袭和迁移的影响,并从上皮间质转化方向研究侵袭和迁移的机制。  方法  体外培养人鼻咽癌细胞HNE-1、CNE-2Z,每株细胞分3组,即空白对照组(control组)、阴性对照组(miR-34a nc组)和过表达miR-34a组(miR-34a mimics组)。荧光定量PCR检测转染后各组细胞miR-34a表达水平。生物信息软件预测miR-34a和FOXM1的靶向关系,荧光定量PCR和Western blotting分析靶向关系。上调miR-34a后,CCK-8法测细胞增殖能力,Transwell、实验测细胞迁移、侵袭能力,Western blotting法测上皮间质转化相关蛋白E-cadherin、Vimentin相对表达水平。  结果  生物信息软件预测miR-34a和FOXM1可能存在靶向关系。在HNE-1、CNE-2Z细胞中,与control组和miR-34a nc组比较,miR-34a mimics组FOXM1的表达下调(HNE-1:0.570±0.041、1.127±0.129、1.125±0.145,F=23.672, P=0.001;CNE-2Z:0.689±0.114、1.966±0.164、1.924±0.087,F=99.599, P<0.001),增殖、迁移和侵袭能力被显著抑制(P < 0.01),E-cadherin表达上调,Vimentin表达下调(P < 0.01)。Control组和miR-34a nc组差异无统计学意义(P>0.05)。  结论  miR-34q通过靶向FOXM1抑制鼻咽癌细胞的增殖、侵袭和迁移,其机制与抑制上皮间质转化有关。 

关 键 词:miR-34a   叉头框蛋白M1   鼻咽癌   细胞增殖   上皮间质转化
收稿时间:2020-11-08

Effects of miR-34a on proliferation and epithelial-mesenchymal transition of nasopharyngeal carcinoma cells by targeting FOXM1
Affiliation:Department of Otorhinolaryngology Head and Neck Surgery, the First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China
Abstract:  Objective  To investigate the effect of miR-34a on the proliferation, invasion and migration of nasopharyngeal carcinoma cells by targeting forkhead box protein M1 (FOXM1) and the mechanism of invasion and migration from the perspective of epithelial-mesenchymal transformation.  Methods  Human nasopharyngeal carcinoma cells (HNE-1 and CNE-2Z) were cultured in vitro. Each cell line was divided into three groups, namely the blank control group (control group), the negative control group (miR-34a nc group) and the overexpression of miR-34a group (miR-34a mimics group). The expression level of miR-34a in each group was detected by qRT-PCR after transfection. The targeted relationship between miR-34a and FOXM1 was predicted by bioinformatics software and then analysed by qRT-PCR and western blot. After overexpression of miR-34a, cell proliferation was detected by CCK-8 assay, cell migration and invasion were detected by Transwell test, and the relative expression levels of invasion- and migration-related proteins such as E-cadherin and Vimentin were detected by western blot.  Results  The possible targeting relationship between miR-34a and FOXM1 was predicted using bioinformatics software. In HNE-1 and CNE-2Z cells, compared with the control group and miR-34a nc group, the expression level of FOXM1 was down-regulated in the miR-34a mimics group (HNE-1: 0.570±0.041, 1.127±0.129, 1.125±0.145, F=23.672, P=0.001; CNE-2Z: 0.689±0.114, 1.966±0.164, 1.924±0.087, F=99.599, P < 0.001); proliferation, migration and invasion abilities were significantly increased (P < 0.01); E-cadherin expression was increased, and Vimentin expression was decreased (P < 0.01). No statistically significant difference was observed between the control group and miR-34a nc group (P>0.05).  Conclusion  miR-34a promotes the proliferation, invasion and migration of nasopharyngeal carcinoma cells by targeting FOXM1, which is associated with the inhibition of epithelial-mesenchymal transformation. 
Keywords:
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