摘要
目的 运用Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-基因突变小鼠,研究Cdc20基因突变在APCmin/＋小鼠结肠癌发生和发展中的作用.方法 通过小鼠杂交得到Cdc20lloxp/＋APCmin/＋ villin-cre＋/-基因突变小鼠和APCmin/＋基因突变小鼠,通过表型分析及组织学分析,比较两组小鼠肠道肿瘤的差异.结果 Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-和APCmin/＋基因突变小鼠肠道肿瘤数分别为（1.2±0.5）、（1.6±0.5）个,差异无统计学意义（t=0.215,P=0.588）;肿瘤最大径分别为（2.7±0.3）、（2.5±0.2） cm,差异无统计学意义（f=0.568,P=0.575）.Cdc20loxp/＋APCmin/＋villin-cre＋/-小鼠肠道肿瘤为腺癌,APCmin/＋小鼠肠道肿瘤为管状腺瘤.结论 Cdc20基因突变可加快APCmin/＋小鼠肠道肿瘤恶变,促进肠道肿瘤发展,但不影响肿瘤数目和大小.
Objective To demonstrate the relationship between Cdc20 mutation and the promotion of colon cancer via Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-compound mutant mice.Methods Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-compound mutant mice and APCmin/＋ mutant mice were generated by mice mating strategy.The colon tumors of two group mice were compared by phenotypic analysis and histology analysis.Results Phenotypic analysis showed that the number of tumors in Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-compound mutant mice group and APCmin/＋ mutant mice group was 1.2±0.5 and 1.6±0.5, respectively （t =0.215, P =0.588）, and the maximum diameter of tumors was （2.7±0.3） cm and （2.5±0.2） cm, respectively （t =0.568, P =0.575）.Pathologic type of Cdc20^loxp/＋APC^min/＋ villin-cre^＋/-compound mutant mice was adenocarcinoma, while that of APCmin/＋ mice was tubular adenoma.Conclusion Cdc20 carrying a null allele can accelerate the promotion of colon cancer in APCmin/＋ mice without influence on the tumor number and size.
出处
《肿瘤研究与临床》
CAS
2016年第3期150-153,共4页
Cancer Research and Clinic
基金
National Natural Science Foundation of China (General Programs)，Innovation and Entrepreneurship Training Program of National College Students of China，国家自然科学基金(面上项目)，国家级大学生创新创业训练计划
