| .miR-101-3p 通过靶向 EZH2 抑制非小细胞肺癌细胞的侵袭和迁移[J].,2024,(24):4643-4648 |
| 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 Inhibits Invasion and Migration of Non-small Cell Lung Eancer Cells by Targeting EZH2 |
| 投稿时间：2023-12-18 修订日期：2024-01-16 |
| DOI：10.13241/j.cnki.pmb.2024.24.007 |
| 中文关键词: miR-101-3p 非小细胞肺癌 EZH2 增殖 迁移 |
| 英文关键词: miR-101-3p non-small cell lung cancer EZH2 Proliferation Migration |
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| 中文摘要: |
| 摘要 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。 |
| 英文摘要: |
| ABSTRACT 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 analyzed 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. |
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