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目的:观察在二甲肼(dimethyl-hydrazine,DMH)诱导小鼠大肠癌的过程中,通过叶酸进行化学干预能否预防肿瘤的发生。方法:以DMH诱发ICR小鼠大肠癌,在诱癌过程中用叶酸进行干预,观察其对肿瘤发生率的影响。定量PCR检测癌基因c-myc转录水平。甲基化特异性PCR(MSP)分析癌基因c-myc启动子区甲基化情况。结果:补充叶酸使小鼠大肠癌的发生率由95%降低至45%;MSP分析9例c-myc表达升高的DMH造模组中有4例发现肿瘤组织DNA启动子区低甲基化,并且发现这4只小鼠的叶酸水平为(71.65±7.04)ng/mL,低于该组其他小鼠(85.75±11.78)ng/mL,P<0.05。结论:通过补充叶酸能有效降低DMH诱发小鼠大肠癌的发生率,其预防肿瘤发生的作用机制与其对基因表达的表观遗传调控有关。
OBJECTIVE: To observe whether the chemical intervention of folic acid can prevent the tumor from occurring in the process of DMH-induced colorectal cancer. Methods: Colorectal cancer was induced by DMH in mice induced by DMH. Folic acid was used as an intervention in the induction of cancer, and its effect on tumor incidence was observed. Quantitative PCR detection of oncogene c-myc transcription level. Methylation-specific PCR (MSP) was used to analyze the methylation of oncogene c-myc promoter region. Results: Folic acid supplementation reduced the incidence of colorectal cancer in mice from 95% to 45%. MSP analysis showed that 9 of 9 DMH patients with elevated c-myc showed hypomethylation in DNA promoter region (71.65 ± 7.04 ng / mL), which was lower than the other mice in this group (85.75 ± 11.78) ng / mL, P <0.05. CONCLUSION: Folic acid supplementation can effectively reduce the incidence of colorectal cancer in DMH-induced mice and its mechanism of preventing tumorigenesis is related to its epigenetic regulation on gene expression.