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作 者:金春晖[1] 黄德芳[4] 谭成[5] 朱晓明[2] 费亚军[3]
机构地区:[1]无锡市中医医院肿瘤科,214001 [2]无锡市中医医院检验科,214001 [3]无锡市中医医院病理科,214001 [4]南通大学第三附属医院内分泌科 [5]江苏省原子医学研究所
出 处:《肿瘤研究与临床》2010年第12期810-813,共4页Cancer Research and Clinic
摘 要:目的观察小鼠肠癌移植瘤在高血糖下的生长并检测瘤体血管内皮生长因子(VEGF)表达以及血清胰岛素样生长因子.1(IGF-1)的变化情况,探讨2型糖尿病(T2DM)是否为促进结直肠癌发生与进展的危险因素。方法建立肠癌移植瘤合并T2DM的小鼠模型,观察移植瘤体积大小变化,5周末处死小鼠检测血清IGF-1及瘤体组织VEGF表达。结果肠癌糖尿病组小鼠瘤体体积[(1628.5±882)mm^3]大于肠癌组小鼠瘤体体积[(1950.2±726)mm^3](P〈0.05),其血清IGF-1[(105.33±32.32)ng/m1]高于正常组[(69.83±25.57)ng/m1]及肠癌组小鼠[(70.17±25.27)ng/m1](P〈0.05),瘤体组织VEGF表达[(70.0±11.5)%]高于肠癌组[(42.9±7.5)%](P〈0.05)。结论T2DM可能为促进肠癌生长的原因之一,其可能机制与血液中升高的IGF-1作用有关,并通过诱导VEGF基因转录,上调VEGF的表达,促使肿瘤组织血管生成,从而导致肿瘤的发生和转移。Objective To observe colorectal tumor' s growth in hyperglycemia mice and its vascular endothelial growth factor (VEGF)' s expression, insulin-like growth factor-1 (IGF-1)' s variation of blood through the experiment, then to ascertain whether type 2 diabetes mellitus (T2DM) danger factors to promote colorectal cancer happen and progress or not. Methods The mouse model of colorectal cancer combined T2DM was established. The volume of tumor was observed. After 5 weeks, all mice were executed and IGF-1 in the blood and the expression of VEGF in the tumor tissue was examined. Results The average tumor volume of colorectal tumor-diabetes group [(1628.5±882) mm^3] were larger than that of colorectal tumor group [(1950.2±726) mm^3] (P 〈0.05), and its expression IGF-1 of blood [(105.33±32.32) ng/ml] were higher than that of the control group [(69.83±25.57) ng/ml] and colorectal tumor group [(70.17±25.27) ng/ml] (P 〈0.05). The expression of VEGF [(70.0±11.5)%] in colorectal tumor-diabetes group were significantly higher than that of colorectal tumor group [(42.9±7.5)%] (P 〈 0.05), too. Conclusion The model of T2DM and transplanted colorectal tumor can be duplicated successfully in ICR mice. Diabetes mellitus may be one reason of promoting colorectal cancer progress. Besides high blood glucose, its mechanism is the high level of IGF-1 which can inhibit apoptosis, promote cell differentiation and hyperplasia, and through inducing VEGF duplicating, heighten its expression, promote the tumor vessel growth, lead to tumor happen and metastasis.
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