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ID:54600963
大小:1.76 MB
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时间:2020-05-03
《叉头样转录因子3的表达及其甲基化状态在肝细胞性肝癌患者中的研究-论文.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、6l6·中华肝脏病杂志2014年8PJ第22卷第8期ChinJHepatol,August2014,Vo1.22,No.8·肝癌·叉头样转录因子3的表达及其甲基化状态在肝细胞性肝癌患者中的研究党珊陈谱张冰斐周健史丽萍I摘要】目的研究叉头样转录因子3(Foxp3)的表达及启动子区甲基化水平在肝细胞性肝癌(HCC)与正常肝组织中的差异及其在HCC发病中的作用。方法使用荧光定量PCR检测39例HCC及13例正常肝组织中Foxp3mRNA水平,通过焦磷酸测序的方法检测其启动子区甲基化水平;组间比较采用秩和检验,相关性分析采用Spearman秩相关,尸<0.05为差异有统计学意义。结果
2、Foxp3mRNA在肝癌组织中相对表达量为8.54士18.30,高于正常肝组织的4.88±14.72,两组比较,Z=一2.770,P:0.0056,差异有统计学意义。Foxp3启动子区A位点的甲基化水平在正常肝组织为90.60±3.50,高于肝癌组织的80.96土20.86,两组比较,=2.I18,尸=0.0339,差异有统计学意义;而正常肝组织和肝癌组织Foxp3启动子区其余B、c、D、E4个位点和整体甲基化水平比较,P值均>0.05,差异均无统计学意义。Foxp3mRNA水平与A位点的甲基化水平相关性分析,,=-0.344,尸=0.046,呈负相关;而其余4个位点与Fox
3、p3mRNA水平均无相关性值均>0.05)。结论Foxp3高表达与Foxp3启动子区A位点低甲基化可能参与肝癌的发生和发展。【关键词】癌,肝细胞;DNA甲基化;叉头样转录因子3ExpressionandmethylationstatusofFoxp3inhumanhepatocellularcarcinomaDangShan木.ChenPu,ZhangBingfei,ZhouJian,ShiLiping,*SecondDepartmentofGastroenterology,ShaanxiProvincialPeople'sHospital,Xi'an710068,China
4、Email:shan.dang@gmail,corn.IA~strm]ObjectiveTogaininsightsintotheroleofforkheadboxprotein3(Foxp3)inthepathogenesisofhepatocellularcarcinoma(HCC)byperformingacomparativeanalysisofFoxp3mRNAexpressionandpromotermethylationstatusinHCCandnormallivertissues.MethodsThirty-nineHCCand13normalliverti
5、ssuespecimenswereevaluatedbyreal-timequantitativePCRandpyrosequencingtomeasuretheexpressionofFoxp3mRNAanddeterminethemethylationstatusofimpromoter,respectively.Statisticalanalysesofthedatawereconductedbyrank-sulntestandSpearman’Srankcorrelationcoeficienttest.ResultsTheHCCspecimensshowedsign
6、ificantlyhighermRNAexpressionofFoxp3(vs.normallivertissues,Z=-2.770,P=0.0056).MoreoveLtheHCCspecimensshowedsignificanthypomethylationoftheFoxp3promotersiteA(VS.normallivertissues,Z:2.118,P:0.0339),andtheFoxp3mRNAlevelwasnegativelycorelatedwimthemethylationofsiteA(rs=一0.344.P=0.046).Noneofth
7、eotherfoursitesintheFoxp3promotershowedasignificantdiferenceinmethylation,andtheoverallmethylationwasnotsignificantlydiferentbetweentheHCCandnormallivertissues.ConclusionOverexpressionandlowmethylationofFoxp3maybeinvolvedintheoncogenicandprogressionproce
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