Slit2促进DMH/DSS诱导的小鼠大肠癌发生发展的实验研究  

Effect of Slit2 on the development of DMH/DSS-induced mouse colorectal cancer

作　　者：陈胜霞[1] 章倩倩[1] 郑力[1] 何晓东[1] 亓翠玲[1] 刘翼龙[1] 王丽京[1] 

机构地区：[1]广东药学院血管生物学研究所,广东广州510006

出　　处：《广东药学院学报》2013年第2期195-198,共4页Academic Journal of Guangdong College of Pharmacy

基　　金：国家自然科学基金(30900764;21005022);国家科技部"973"项目国家重点基础研究发展计划(2010CB529702)

摘　　要：目的研究Slit2基因在小鼠大肠癌形成过程中的作用。方法分别用Slit2过表达转基因小鼠及C57小鼠构建DMH/DSS诱导的大肠癌模型,观察二者大肠肿瘤的数目和总负荷。结果成功构建了DMH/DSS诱导的肠炎相关性大肠癌模型;与C57小鼠相比,Slit2过表达转基因小鼠在诱导13周后,大肠肿瘤数目和总负荷明显增加。结论 Slit2过表达能促进小鼠大肠癌的发生发展。Objective To investigate the role of Slit2 on the development of large intestine cancer in mice.Methods The mouse model of large intestine cancer was established with DMH/DSS treatment.The number and volume of large intestine cancer were measured in Slit2-overexpressing transgenic mice and C57 mice.Results The animal model of colorectal cancer model was successfully established.Compared with C57 mice,the number and volume of large intestine cancer were significant increased in Slit2-overexpressing transgenic mice when treated with DMH/DSS after 13 weeks.Conclusion Slit2 may promote pathogenesis of large intestine cancer in mice.

关 键 词：Slit2基因 转基因小鼠 大肠癌 化学诱导 

分 类 号：R735.34[医药卫生—肿瘤]