张延慧,王涛,刘靖,刘翠云,李培峰,王昆.长链非编码RNA肿瘤抑制因子对阿霉素诱导的A549细胞凋亡的影响[J].转化医学杂志,2019,8(2):71-74
长链非编码RNA肿瘤抑制因子对阿霉素诱导的A549细胞凋亡的影响
The effect of long non-coding RNA TIF on Doxorubicin-induced apoptosis of A549 cells
  
DOI:
中文关键词:  长链非编码RNA  A549细胞  线粒体分裂  细胞凋亡
英文关键词:Long no-coding RNA( lncRNA)  A549 cells  Mitochondrial division  Apoptosis
基金项目:青岛市博士后应用研究项目(2016069)
作者单位
张延慧 青岛大学转化医学研究院 
王涛 青岛大学转化医学研究院 
刘靖 青岛大学转化医学研究院 
刘翠云 青岛大学转化医学研究院 
李培峰 青岛大学转化医学研究院 
王昆 青岛大学转化医学研究院 
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中文摘要:
      目的 探究长链非编码RNA(long non-coding RNA,lncRNA)对阿霉素(doxorubicin,DOX)诱导的肺癌细胞系A549细胞凋亡的影响。方法 采用高通量lncRNAs基因芯片技术,筛选出2 μmol/L的DOX处理组中差异表达的lncRNAs,同时通过实时荧光定量PCR技术进行复筛,得到差异表达最显著的lncRNA,lnc-ZMYM6-2-1,我们命名为lncRNA肿瘤抑制因子(tumor inhibitory factor,TIF)。进一步比较19对肺癌组织和癌旁组织样本中lncRNA TIF的表达差异。通过MitoTracker线粒体染色法检测lncRNA TIF对细胞线粒体分裂与融合的影响,通过流式细胞仪检测lncRNA TIF对细胞凋亡的影响。结果 ①通过基因芯片与实时荧光定量PCR检测发现,与不做处理的对照组相比,DOX处理组中lncRNA TIF表达显著上调(n=3;t=6.4,P<0.01);②与癌旁组织比较lncRNA TIF在肺癌组织样本中低表达(n=19;t=18.5,P<0.01);③敲低lncRNA TIF能够抑制DOX引起的线粒体分裂和细胞凋亡。结论 化疗药物DOX能够诱导lncRNA TIF的表达进而诱导细胞凋亡,其机制可能通过促进线粒体分裂来促进细胞凋亡。
英文摘要:
      Objective To investigate the effect of long non-coding RNA (lncRNA) on apoptosis of A549 cells induced by doxorubicin (DOX). Methods By using the high-through-put lncRNAs gene chip technology, we screened the differentially expressed lncRNAs in the 2 μmol/L DOX treated group compared with the control group and the re-screening was performed by real-time fluorescent quantitative PCR. The significantly differentially expressed lncRNA, lnc-ZMYM6-2-1, we named lncRNA tumor inhibitor factor (TIF). The expression of lncRNA TIF in 19 lung cancer tissues and adjacent tissues were further compared. Then we detect the effect of lncRNA TIF on cell mitochondrial division, fusion and apoptosis by MitoTracker mitochondrial staining and flow cytometry. Results By the result of gene chip and real-time fluorescent quantitative PCR, it was found that the expression of lncRNA TIF was significantly up-regulated in the DOX-treated group compared with the control group (n=3;t=6.4,P<0.01). LncRNA TIF was down-regulated in lung cancer tissue samples (n=19;t=18.5,P<0.01) compared with the adjacent tissues. Knockdown of lncRNA TIF inhibits DOX-induced mitochondrial division and apoptosis. Conclusion The DOX can induce the expression of lncRNA TIF and induce apoptosis, which may promote apoptosis by promoting mitochondrial division.
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