| 潘 琪,王守峰,杨 立,吴俊伟,茅乃权.Cav-1通过增加IncRNA HOTAIR的表达促进非小细胞肺癌细胞增殖[J].,2019,19(6):1055-1059 |
| Cav-1通过增加IncRNA HOTAIR的表达促进非小细胞肺癌细胞增殖 |
| Cav-1 Promotes the Cell Proliferation of Lung Cancer by Increasing the IncRNAHOTAIR Expression |
| 投稿时间：2018-08-06 修订日期：2018-08-30 |
| DOI：10.13241/j.cnki.pmb.2019.06.011 |
| 中文关键词: Cav-1 IncRNA HOTAIR 肺癌 细胞增殖 |
| 英文关键词: Cav-1 IncRNA HOTAIR Lung cancer Cell proliferation |
| 基金项目:广西壮族自治区卫生和计划生育委员会自筹经费科研课题(Z2016486) |
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| 中文摘要: |
| 摘要 目的：探讨Cav-1对非小细胞肺癌(NSCLC)细胞增殖的影响及其分子机制。方法：取我院收治的2017年1月至2018年1月15例NSCLC患者手术切除的肺组织，并获取肺癌旁组织15例。实时定量PCR检测其中Cav-1和lncRNA HOTAIR的表达。进一步检测Cav-1和lncRNA HOTAIR在各肺癌细胞系中的表达。采用脂质体3000介导将siCAV-1和pcDNA3.1/CAV-1转染入NSCLC细胞系中，实时定量PCR检测lncRNA HOTAIR的表达，CCK-8检测细胞增殖。随后，将siHOTAIR以及pcDNA3.1/ HOTAIR转染入CAV-1过表达的NSCLC细胞系中，CCK-8检测细胞增殖情况。结果：NSCLC患者手术切除的肺组织中CAV-1 mRNA和HOTAIR lncRNA的表达均显著高于其在癌旁组织(P＜0.001)。与健康人肺组织上皮细胞系(NuLi-1)相比，各肺癌细胞系中CAV-1 mRNA和HOTAIR lncRNA的表达均显著增加，鳞状细胞癌细胞系(SK-MES-1)除外。siCAV-1显著降低NSCLC中CAV-1的表达(P0.01)以及其增殖能力，而pcDNA3.1/CAV-1显著增加NSCLC中CAV-1的表达(P＜0.01)以及其增殖。与对照siRNA相比，siCAV-1显著降低HOTAIR lncRNA的表达(P＜0.05)。与对照质粒相比，pcDNA3.1/CAV-1显著增加HOTAIR lncRNA的表达(P＜0.01)。siHOTAIR可显著抑制NSCLC细胞增殖(P＜0.05)，且可明显取消pcDNA3.1/CAV-1转染对NSCLC细胞增殖的促进作用(P＜0.05)，而pcDNA3.1/HOTAIR可显著增加NSCLC细胞增殖(P＜0.05)，且CAV-1过表达可增强pcDNA3.1/HOTAIR对NSCLC细胞增殖的促进作用(P＜0.05)，而siCAV-1转染可抑制pcDNA3.1/HOTAIR对NSCLC细胞增殖的促进作用。结论：CAV-1通过上调lncRNA HOTAIR的表达促进肺癌细胞的增殖。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the effect and molecular mechanism of Cav-1 on the proliferation of non-small cell lung cancer(NSCLC) cells. Methods: Surgically removed lung tissue was obtained from 15 cases of NSCLC patients who admitted in our hospital from January 2017 to January 2018 and 15 cases of corresponding paracancer tissue was also obtained. The expressions of CAV-1 and lncRNA HOTAIR were detected by real-time quantitative PCR (qRT-PCR). The siCAV-1 and pcDNA3.1/CAV-1 were transfected into NSCLC cells by Lipofectamine3000. Expression of lncRNA HOTAIR was tested by qRT-PCR, cell proliferation was measured by CCK-8. Then, siHOTAIR and pcDNA3.1/ HOTAIR were transfected into CAV-1-overexpressed NSCLC cells, the cell proliferation was measured by CCK-8. Results: The expressions of CAV-1 and lncRNA HOTAIR in NSCLC tissue were higher than those in the paracancer tissue(P<0.001). Compared with normal lung tissue epithelial cell lines(NuLi-1), the expressions of CAV-1 and lncRNA HOTAIR in multifarious lung cancer cell lines were also increased, besides that in squamous cell cancer cell line(SK-MES-1). The siCAV-1 significantly reduced the CAV-1 expression(P<0.01) and cell proliferation of NSCLC cells. The pcDNA3.1/CAV-1 significantly increased the CAV-1 expression(P<0.01) and cell proliferation of NSCLC cells. The siHOTAIR reduced cell proliferation of NSCLC cells, whereas pcDNA3.1/CAV-1 increased siHOTAIR-induced cell proliferation. pcDNA3.1/HOTAIR increased cell proliferation, and pcDNA3.1/CAV-1 also enhanced pcDNA3.1/HOTAIR-induced cell proliferation which was inhibited by siCAV-1 transfection. Conclusion: CAV-1 may promote the proliferation of NSCLC cells by regulating lncRNA HOTAIR expression. |
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