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S-腺苷甲硫氨酸抑制大肠癌细胞生长的实验研究
引用本文:罗瑾,李燕妮,耿鑫,张维铭. S-腺苷甲硫氨酸抑制大肠癌细胞生长的实验研究[J]. 生物医学工程与临床, 2011, 15(2): 183-186,188
作者姓名:罗瑾  李燕妮  耿鑫  张维铭
作者单位:1. 天津医科大学,生物化学教研室,天津,300070
2. 天津市口腔医院中心实验室,天津,300041
基金项目:国家自然科学基金,天津市高校科技发展计划项目,天津医科大学科研基金项目
摘    要:
目的探讨S-腺苷甲硫氨酸(SAM)对人大肠癌细胞生长的抑制作用及抑癌机制。方法用SAM对大肠癌细胞系HT-29进行处理,使其癌基因c-myc和H-ras启动子区域甲基化。用噻唑蓝(MTT)法检测肿瘤细胞生长状态;甲基化特异性聚合酶链反应(PCR)(MSP)法检测c-myc和H-ras启动子区域甲基化状态;细胞免疫荧光染色检测C-MYC和H-RAS蛋白的表达情况。结果大肠癌细胞系HT-29经SAM处理后,癌基因c-myc和H-ras启动子区域重新出现甲基化。经SAM处理的大肠癌细胞组与对照组相比,细胞生长受到明显抑制,差异有统计学意义(P<0.05);C-MYC和H-RAS蛋白表达明显降低,差异有统计学意义(P<0.05)。结论 SAM能使HT-29中癌基因c-myc和H-ras启动子区域重新甲基化,降低C-MYC和H-RAS蛋白的表达水平,且有效抑制了肿瘤细胞的生长,从而为肿瘤治疗提供了新的靶点。

关 键 词:S-腺苷甲硫氨酸  重新甲基化  大肠癌细胞

Experimental study on inhibition of colorectal cancer cell growth by S-adenosylmethionine
LUO Jin,LI Yan-ni,GENG Xin,ZHANG Wei-ming. Experimental study on inhibition of colorectal cancer cell growth by S-adenosylmethionine[J]. Biomedical Engineering and Clinical Medicine, 2011, 15(2): 183-186,188
Authors:LUO Jin  LI Yan-ni  GENG Xin  ZHANG Wei-ming
Affiliation:1.Key Laboratory of Immune Microenvironment and Diseases,Ministry of Education,Department of Biochemistry,Tianjin Medical University,Tianjin 300070,China;2.Central Laboratory,Tianjin Stomatology Hospital,Tianjin 300041,China)
Abstract:
Objective To explore the inhibitory effects of S-adenosylmethionine(SAM) on the growth of colorectal cancer cells and the underlying mechanisms.Methods The oncogenes c-myc and H-ras promoter regions of HT-29 cells were methylated by treatment with SAM and tumor cell growth was evaluated by 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide(MTT) assay.The degree of methylation of c-myc and H-ras promoter regions was detected by methylation-specific PCR(MSP) and the expression of C-MYC and H-RAS proteins was determined by cytoimmunofluorescence.Results The c-myc and H-ras promoter regions in colorectal cancer cells were methylated after treatment with SAM.Compared with the control group,the growth of the colorectal cancer HT-29 cells treated with SAM were significantly inhibited(P 0.05) and the expressions of C-MYC and H-RAS proteins were obviously down-regulated(P 0.05).Conclusion It was demonstrated that SAM could lead to the re-methylation of the promoter of oncogenes c-myc and H-ras in colorectal caner HT-29 cells,which resulted in decreased expressions of C-MYC and H-RAS proteins,and thus effectively inhibited the growth of cancer cells.
Keywords:S-adenosylmethionine  re-methylation  colorectal cancer cell
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