首页|miR-101-3p通过靶向EZH2抑制非小细胞肺癌细胞的侵袭和迁移

miR-101-3p通过靶向EZH2抑制非小细胞肺癌细胞的侵袭和迁移

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目的:研究miR-101-3p在非小细胞肺癌(NSCLC)中的生物学功能和潜在机制。方法:使用UALCAN平台中的基于TCGA数据库分析肺腺癌和正常组织中miR-101-3p的表达,Kaplan-Meier生存分析miR-101-3p高表达组和低表达组的生存率差异。qRT-PCR检测NSCLC细胞系A549、H1299、H1975、PC-9和肺正常上皮细胞BEAS-2B中miR-101-3p的表达水平。将miR-101-3p模拟物转染A549和H1299细胞分为miR-101-3p模拟物组和miR-NC对照组,CCK-8法检测细胞活力,Transwell小室检测细胞迁移和侵袭能力;通过生物信息学分析和荧光素酶报告基因寻找和分析miR-101-3p的靶基因和结合位点;EZH2过表达A549细胞,CCK-8和伤口愈合实验检测细胞活力和迁移能力。结果:TCGA数据库中肺腺癌组织中miR-101-3p低表达,且与较差的生存预后相关,同样,与BEAS-2B相比,miR-101-3p在NSCLC细胞中低表达(P<0。05)。此外,转染miR-101-3p模拟物抑制A549和H1299细胞的增殖、迁移和侵袭(P<0。05)。EZH2是miR-101-3p的靶基因,miR-101-3p模拟物转染细胞后EZH2表达水平降低,EZH2过表达逆转了 miR-101-3p在A549细胞中的细胞活力和迁移能力的抑制作用(P<0。05)。结论:miR-101-3p可能通过靶向EZH2抑制NSCLC细胞增殖和迁移。
miR-101-3p Inhibits Invasion and Migration of Non-small Cell Lung Eancer Cells by Targeting EZH2
Objective:To study the biological function and potential mechanism of miR-101-3p in non-small cell lung cancer(NSCLC).Methods:The expression of miR-101-3p in lung adenocarcinoma and normal tissues was analyzed by TCGA database in UALCAN platform,and the difference of survival rate between high expression group and low expression group of miR-101-3p was ana-lyzed by Kaplan-Meier survival analysis.The expression levels of miR-101-3p in NSCLC cell lines A549,H1299,H1975,PC-9 and lung normal epithelial cells BEAS-2B were detected by qRT-PCR.A549 and H1299 cells transfected with miR-101-3p mimic were divided into miR-101-3p mimic group and miR-NC control group.Cell viability was detected by CCK-8,and cell migration and invasion were detected by Transwell.The target genes and binding sites of miR-101-3p were found and analyzed by bioinformatics analysis and luciferase reporter gene.EZH2 was overexpressed in A549 cells.CCK-8 and wound healing assay were used to detect cell viability and migration ability.Results:Low expression of miR-101-3p in lung adenocarcinoma tissues in the TCGA database and its association with poorer survival prognosis.Similarly,compared with BEAS-2B,the expression of miR-101-3p was lower in NSCLC cells(P<0.05).In addition,transfection of miR-101-3p mimic inhibited the proliferation,migration and invasion of A549 and H1299 cells(P<0.05).EZH2 is a target gene of miR-101-3p.The expression level of EZH2 was reduced after transfection of miR-101-3p mimics into cells,and EZH2 overexpression reversed the inhibitory effect of miR-101-3p on cell viability and migration ability in A549 cells(P<0.05).Conclusion:MiR-101-3p may inhibit the proliferation and migration of NSCLC cells by targeting EZH2.

miR-101-3pnon-small cell lung cancerEZH2ProliferationMigration

姬翔、王娟、陈晓霞、吴文婷、徐月亮、刘勇世

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空军军医大学第二附属医院胸腔外科 陕西西安 710038

空军军医大学第二附属医院呼吸科 陕西西安 710038

miR-101-3p 非小细胞肺癌 EZH2 增殖 迁移

2024

现代生物医学进展
黑龙江省森工总医院 哈尔滨医科大学附属第四医院

现代生物医学进展

CSTPCD
影响因子:0.755
ISSN:1673-6273
年,卷(期):2024.24(24)