摘要
目的 :探讨幽门螺杆菌 (Hp)感染特别是其细胞毒素相关基因 (cagA因子 )与胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1蛋白表达异常的关系 ,从而从分子水平初步探讨cagA是否为一致癌因子及其可能的致癌的机理。方法 :1、利用血抗Hp IgG、RUT、PCR Hp DNA 3种方法检测 2 70例病人的Hp感染情况及cagA+ Hp感染情况 ;2、利用免疫组化S P法检测胃癌演化系列胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1蛋白的表达 ;3、利用SPSS统计软件包作统计学分析处理。结果 :1、在CSG、CAG、IM阶段 ,Hp感染促进胃粘膜中bcl 2、Bax的表达 ,cagA因子促进bcl 2、Bax、p2 1 WAF1、p16 MTS1的表达 ,(P <0 0 5 ) ;在胃癌阶段 ,Hp感染与胃腺癌粘膜中bcl 2、p2 1 WAF1、p16 MTS1的低表达相关 (P <0 0 5 ) ,但与cagA因子无关 (P >0 0 5 ) ;2、在男性CSG、CAG、IM系列胃粘膜中bcl 2、Bax表达先高后低 ,与cagA+ Hp感染率呈正相关 ,而 p16 MTS1、p2 1 WAF1表达先低后高 ,与cagA+ Hp感染率呈负相关 (P <0 0 5 )。结论 :Hp的cagA因子可能通过影响癌前病变患者胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1的表达 ,成为胃腺癌发生的“启动子”之一 ;Hp可能通过非cagA因子途径影响bcl 2、p2 1 WAF1、p16 MTS1的表达 。
Objective:To investigate the association between the aberrant expression of the bcl 2, Bax, p16 MTS1 and p21 WAF1 proteins and infection of Helicobacter pylori(Hp) in the multiple process of gastric carcinogenesis Then, to explore the possible carcinogenic mechanisms of Hp and its cagA factor in the molecular level Methods:1 The Hp in specimens from 270 patients with chronic gastritis or gastric adenocarcinoma(GAC) were detected by PCR、RUT and the serum anti Hp IgG detection three methods, its cagA gene was detected by PCR 2 The bcl 2, Bax, p16 and p21 proteins in gastric biopsy specimens were detected by immunohistochemical methods(with S P kit) 3 The data were analyzed by computer with the SPSS statistic software Results:1 Hp infection would promote the expression of Bax, bcl 2 in gastric subjects with chronic superficial gastritis(CSG), chronic atrophic gastritis(CAG) or intestinal metaplasia(IM), and the cagA factor stimulated the expression of Bax, bcl 2, p16 and p21 in the CSG, CAG or IM subjects(P< 0 05) The correlation between Hp infection and the lower expression of bcl 2, p21 and p16 in GAC subjects was seen(P< 0 05), no correlation was noted with cagA factor(P >0 05); 2 In the CSG, CAG and IM sequence of male patients, the expression of Bax, bcl 2 went up in the CAG patients, and then went down in the IM patients, the positive correlation between the expression of Bax, bcl 2 and the rates of cagA +Hp infection was noted (P< 0 05) Meanwhile, the expression of p16, p21 went down in the CAG patients, and then went up in the IM patients (P< 0 05), the negative correlation between the expression of p16, p21 and the rates of cagA +Hp infection was seen (P< 0 05) Conclusions:The cagA factor may become one of the promotors of gastric carcinogenesis through influencing the expression of Bax, bcl 2, p12 and p21 in gastric mucosa with CSG, CAG or IM Hp may involve in the development of GAC through influencing the expression of bcl 2, p16 and p21 via non cagA factor pathways
出处
《癌症》
SCIE
CAS
CSCD
北大核心
2000年第5期419-422,共4页
Chinese Journal of Cancer
基金
福建省科委基金!(No 98-Z- 16 8)资助
关键词
幽门螺杆菌
胃肿瘤
CAGA因子
原癌基因
Helicobacter pylori
CagA gene
Stomach neoplasms
Bax
bcl 2
p16 MTS1
p21 WAF1
