CAJ | 학술논문

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)mm3]大于肠癌组小鼠瘤体体积[(1950.2±726)mm3](P<0.05),其血清IGF-1[(105.33±32.32)ng/ml]高于正常组[(69.83±25.57)ng/ml]及肠癌组小鼠[(70.17±25.27)ng/ml](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.
목적 관찰소서장암이식류재고혈당하적생장병검측류체혈관내피생장인자(VEGF)표체이급혈청이도소양생장인자-1(IGF-1)적변화정황,탐토2형당뇨병(T2DM)시부위촉진결직장암발생여진전적위험인소.방법 건립장암이식류합병T2DM적소서모형,관찰이식류체적대소변화,5주말처사소서검측혈청IGF-1급류체조직VEGF표체.결과 장암당뇨병조소서류체체적[(1628.5±882)mm3]대우장암조소서류체체적[(1950.2±726)mm3](P<0.05),기혈청IGF-1[(105.33±32.32)ng/ml]고우정상조[(69.83±25.57)ng/ml]급장암조소서[(70.17±25.27)ng/ml](P<0.05),류체조직VEGF표체[(70.0±11.5)%]고우장암조[(42.9±7.5)%](P<0.05).결론 T2DM가능위촉진장암생장적원인지일,기가능궤제여혈액중승고적IGF-1작용유관,병통과유도VEGF기인전록,상조VEGF적표체,촉사종류조직혈관생성,종이도치종류적발생화전이.
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) mm3] were larger than that of colorectal tumor group [(1950.2±726) mm3] (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.