三联脆组基因对胰腺癌细胞增殖及凋亡的影响  

The effect of fragile histidine triad gene on the growth and apoptosis of pancreatic adenocarcinoma cells

作　　者：蔡清萍[1] 李海倩[1] 付志仁[1] 王梁华[2] 焦炳华[2] 徐冠南[1] 张国治南 

机构地区：[1]第二军医大学长征医院普外科,上海200003 [2]第二军医大学基础部毒理教研室 [3]第二军医大学长征医院普外科消化科,上海200003

出　　处：《中华消化杂志》2001年第7期423-425,共3页Chinese Journal of Digestion

摘　　要：目的　研究三联脆组基因 (fragilehistidinetriad ,FHIT)对胰腺癌细胞增殖的影响 ,探讨FHIT基因对胰腺癌增殖的抑癌机制。方法　通过脂质体介导的方法将 pRC/CMVFHIT质粒转染有FHIT全基因丢失的胰腺癌 1990细胞株。用RT PCR及Western blot方法对获得G418抗性细胞进行外源性FHIT基因整合及表达的鉴定。对导入有外源性FHIT基因表达的细胞 (1990 pFHIT)进行细胞生长特征及裸鼠致瘤性分析。经光镜及电镜对 1990pFHIT进行观察 ,并对其进行DNA片段化分析。结果　转染FHIT基因的 1990细胞 ,有外源性FHIT基因的整合及表达 ,其增殖活性明显减弱 ,裸鼠致瘤性明显降低或消失。 1990pFHIT细胞中存在明显的凋亡现象。结论　导入外源性的FHIT基因 ,通过某种途径诱导胰腺癌细胞的凋亡 ,从而抑制肿瘤细胞的恶性增殖。Objective To study the effect of fragile histidine triad (FHIT) gene on pancreatic adenocarcinoma cells growth and tumorigenicity and explore the mechanism of FHIT gene in suppressing the deve lopment of pancreatic adenocarcinoma. Methods By the method of liposome transfection, pRC/CMV FHIT plasmid was transfected into 1990 cell lines which lose all of FHIT gene. Integration and expression of exogenous FHIT gene were confirmed by RT PCR and Western blot technique. 1990 pFHIT cell growth was observed in regular culture medium and tumorigenicity in nude mice. Its DNA was analyzed by electrophoresis. Results The growth of the cells transfected with FHIT gene (named as 1990 pFHIT cells) was suppressed significantly, and the tumorigenicity of the 1990 pFHIT cells was dramatically inhibited in nude mice as compared with that of the parental 1990 cells. Significantly increased apoptosis in 1990 pFHIT was found. Conclusions The growth and tumorigenicity of pancreatic adenocarcinoma cell can be inhibited by transduced exogenous FHIT gene. It's spectulated that FHIT suppress the development of pancreatic adenocarcinoma by the path of apoptosis.

关 键 词：三联脆组基因 胰腺癌 基因表达 细胞凋亡 细胞增殖 

分 类 号：R735.9[医药卫生—肿瘤]