哈萨克族食管癌中Cdc42，Survivin，P16基因启动子区甲基化状态与其mRNA表达改变的研究
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摘要
目的:研究新疆哈萨克族食管癌中Cdc42,Survivin,P16基因启动子区甲基化状态与其mRNA表达改变的关系。方法:用RT-PCR方法测定mRNA表达,甲基化特异PCR方法检测DNA启动子区甲基化。结果: Cdc42基因在36对癌及癌旁组织中,癌组织表达明显高于癌旁组织的有14例,占39%。而癌组织和癌旁组织该基因启动子区的甲基化无明显差异,均表现为高甲基化状态。Survivin基因在36对癌及癌旁组织中,癌组织表达明显高于癌旁组织的有25例,占69%。癌组织和癌旁组织启动子区多为部分甲基化状态,其中25对癌组织表达高于癌旁组织标本中,癌组织甲基化扩增量明显低于癌旁组织的有15例,占60%。P16基因在36对癌及癌旁组织中,癌旁组织表达明显高于癌旁组织的有19例,占53%而癌组织和癌旁组织该基因启动子区的甲基化无明显差异,多表现为非甲基化状态。结论: Cdc42基因在癌组织和癌旁组织均表现为高甲基化状态,P16基因在癌组织和癌旁组织多表现为非甲基化状态。新疆哈萨克族食管癌中Cdc42,P16基因mRNA表达的差异可能与这两个基因的甲基化状态没有关系,另存在其它机制,有待进一步研究。Survivin基因在25对癌组织表达高于癌旁组织标本中,癌组织甲基化扩增量明显低于癌旁组织的有15例,占60%,新疆哈萨克族食管癌中Survivin基因启动子区的甲基化状态可能是其基因高表达原因之一。
Objective: To study the expression of Cdc42,Survivin,P16 and promoter methylation in Hazak’s esophageal cancer. Methods: Cdc42,Survivin,P16 expression and Cdc42,Survivin,P16 promoter methylation, was detected in 36 cases of esophageal cancer tissues and tumor-adjacent normal tissues by Reverse Transcription Polymerase Chain Reaction and methylation-specific PCR (MSP). Results: In detected oncogenes, the expression of Cdc42 gene increased in 17 cases compared with that in tumor-adjacent normal tissues within 36 cases; 25 cases show higher expression level for Survivine,19 cases lower than normal tissues of P16。promoter methylation was observed in esophageal cancer tissues and tumor-adjacent normal tissues。promoter methylation does not show changes in Cdc42 and p16 gene ;15 cases cancer show low methylation than tumor-adjacent normal tissues for Survivine .Conclusion: It is suggested that the cell apoptosis and cell cycle resulted from the abnormal expression of Cdc42,Survivine,P16 gene affects the occurrence of Hazak’s esophageal cancer,but the Cdc42,P16 promoter methylation is not relation with the expression。promoter methylation is less importmant in Cdc42,P16 gene than in other gene ,Survivine gene aberrant methylation could be the molecular and genetic alteration in in Hazak’s esophageal cancer.
Objective: To study the expression of Cdc42,Survivin,P16 and promoter methylation in Hazak’s esophageal cancer. Methods: Cdc42,Survivin,P16 expression and Cdc42,Survivin,P16 promoter methylation, was detected in 36 cases of esophageal cancer tissues and tumor-adjacent normal tissues by Reverse Transcription Polymerase Chain Reaction and methylation-specific PCR (MSP). Results: In detected oncogenes, the expression of Cdc42 gene increased in 17 cases compared with that in tumor-adjacent normal tissues within 36 cases; 25 cases show higher expression level for Survivine,19 cases lower than normal tissues of P16。promoter methylation was observed in esophageal cancer tissues and tumor-adjacent normal tissues。promoter methylation does not show changes in Cdc42 and p16 gene ;15 cases cancer show low methylation than tumor-adjacent normal tissues for Survivine .Conclusion: It is suggested that the cell apoptosis and cell cycle resulted from the abnormal expression of Cdc42,Survivine,P16 gene affects the occurrence of Hazak’s esophageal cancer,but the Cdc42,P16 promoter methylation is not relation with the expression。promoter methylation is less importmant in Cdc42,P16 gene than in other gene ,Survivine gene aberrant methylation could be the molecular and genetic alteration in in Hazak’s esophageal cancer.
引文
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[8]黄琼晓,金帆,黄荷凤.DNA甲基化的研究方法学[J].国外医学遗传学分册, 2004, 27 (6):354-358.
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[16]Keeney S,Bauer TL.Epidemiology of adenocarcinoma of the esophagogastric junction [J]. Surg Oncol Clin N Am. 2006,15(4):687-96.
[17]Zhang YM. The distribution of esophageal cancer in Xinjiang[J].Xinjiang Yixueyuan Xuebao,1988,11(2):139-145.
[18]Whelan SL,Parkin DM,Masuyer E,et al. Histogarms depictingrates of cancer age standard- ized to the world population by site and sex,In:international Agecy for Research on cancer,Patterns of Cancer in Five Continents.Lyon:I.A.R.C.[J] Sciemtific Publications,No 102,1990.
[19]Munoz N. Epedemioligical aspects of esophageal cancer [J].Endoscopy, 1993, 23:609 -612.
[20]库热西·玉努斯,王丽容,赵学信,等.新疆哈萨克族食管癌APC抑癌基因等位基因杂合缺失和点突变研究[J].新疆医科大学学报,1999,22(2):79-81.
[21]沈望珍,赵学信,王丽容.新疆地区食管癌组织ras基因突变的研究[J].新疆医科大学学报,1999,22(4):233-235.
[22]沈望珍,王丽蓉,赵学信,等。食管癌组织p53抑癌基因等位基因杂合缺失及突变的研究[J].新疆医学院学报,1998,21(1):10-14.
[23]库热西·玉努斯,王丽容,斯坎德尔·白克力,等.新疆哈萨克族食管癌p16抑癌基因缺失及其表达的研究[J].新疆医科大学学报,2003,23(1):10-12.
[24]赵学信,王丽蓉,沈望珍.哈萨克族食管癌患者3号染色体短臂3p24等位基因杂合缺失的研究[J].新疆医学院学报,1996,19(3):143-145.
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