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作 者:刘盼[1] 董稚明[1] 董玉然[1] 郭炜[1] 王益民[2] 郭艳丽[1]
机构地区:[1]河北医科大学第四医院河北省肿瘤研究所病理研究室,河北石家庄050011 [2]秦皇岛市第一医院普外科,河北秦皇岛066000
出 处:《中华肿瘤防治杂志》2010年第15期1199-1202,共4页Chinese Journal of Cancer Prevention and Treatment
基 金:河北省强势特色学科基金(冀教高[2005]52号)
摘 要:目的:探讨食管鳞状细胞癌(ES-CC)组织中转化生长因子β受体Ⅰ、Ⅱ(TβRⅠ、Ⅱ)基因启动子甲基化及其mRNA表达的关系。方法:改进的甲基化特异性聚合酶链式反应(MSP)和逆转录-聚合酶链反应(RT-PCR)技术检测65例ESCC及59例癌旁组织中TβRⅠ和TβRⅡ基因启动子的甲基化状态和41例ESCC及15例癌旁组织中TβRⅠ和TβRⅡ基因mRNA的表达水平,分析2个基因启动子甲基化与临床参数和mRNA表达的关系。结果:TβRⅠ在ES-CC和癌旁组组的甲基化率分别为52.3%(34/65)和40.7%(24/59),差异无统计学意义,χ2=1.680,P=0.195。TβRⅡ在ESCC和癌旁组组的甲基化率分别为70.8%(46/65)和47.5%(28/59),ESCC组的甲基化率显著高于癌旁组,χ2=6.984,P=0.008。TβRⅠ和TβRⅡ基因启动子甲基化与临床资料无关,P>0.05。ESCC组TβRⅠ和TβRⅡmRNA表达水平均明显低于癌旁组织(t1=-3.393,P1=0.001;t2=-2.358,P2=0.022),ESCC组中发生甲基化和未发生甲基化的mRNA表达水平差异无统计学意义,t1=-1.287,P1=0.206;t2=-0.922,P2=0.362。结论:TβRⅠ基因甲基化可能与ESCC的发生、发展无关,而TβRⅡ基因启动子甲基化可能是引起基因转录失活,导致ESCC形成的原因之一。OBJECTIVE:To investigate the methylation status in promoters and mRNA expressions of transforming growth factor β receptor Ⅰ and Ⅱ(TβRⅠ,Ⅱ) genes in esophageal squamous cell carcinoma(ESCC).METHODS:Modified methylation specific PCR(MSP) was used to detect the methylation status of TβR Ⅰ and Ⅱgene promoters in 65 ESCC and their 59 adjacent non-cancerous tissues.The expression of TβRⅠ and Ⅱ mRNA were also determined by reverse transcriptase PCR in 41 ESCC and their 15 adjacent non-cancerous tissues.The correlation between methylation and mRNA expressions of the two genes and clinical data was analyzed.REULTS:For TβR Ⅰ,methylation was detected in 34 of 65 (52.3%) ESCC tissues and 24 of 59(40.7%) adjacent non-cancerous tissues,and there was no significantly statistical differences between them (χ^2=1.680,P=0.195).For TβR Ⅱ,methylation was detected in 46 of 65 (70.8%) ESCC tissues and 28 of 59 (47.5%) adjacent non-cancerous tissues,and the methylation rate of ESCC tissues was significantly higher than that of the others(χ^2=6.984,P=0.008).No correlation was found between methylation status of TβR Ⅰ and Ⅱ genes and the clinical data (P〈0.05).The expressions level of TβR Ⅰ and Ⅱ gene mRNA in the ESCC group were significantly lower compared with those in the adjacent non-cancerous group (t1=-3.393,P1=0.001;t2=-2.358,P2=0.022).No significant differences were found between methylated and unmethylated ESCC (t1=-1.287,P1=0.206;t2=-0.922,P2=0.362).CONCLUSIONS:The methylation of TβR Ⅰ has no effect on the formation and development of ESCC.However,The methylation of TβR Ⅱ promoter maybe is one of the reasons which cause the gene transcription inactivation and the development of ESCC.
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