中文摘要：

目的探讨甲基化药物S-腺苷甲硫氨酸（S-adenosyl-L-methionine,SAM）对结直肠癌细胞株SW620和LoVo体外克隆形成能力及对细胞生长周期和凋亡的影响。方法甲基化药物SAM处理结直肠癌细胞株SW620和LoVo 6 d后,采用平板克隆形成实验检测SAM对细胞分裂形成克隆的能力,采用流式细胞术检测SAM对细胞生长周期中各个阶段的影响及对凋亡的影响。以SAM的同型异构体S-腺苷高半胱氨酸（S-adeno-syl-L-homocysteine,SAH）处理组细胞及空白处理组细胞作为对照。结果与空白处理组和SAH处理组细胞相比,SAM处理后两种结直肠癌细胞的克隆形成能力明显减弱,差异有统计学意义（LoVo：P〈0.001;SW620：P〈0.001）。流式细胞术检测结果显示,与SAH处理组细胞比较,SAM处理后LoVo细胞发生了S期阻滞（P〈0.001）,SW620细胞发生了G1期阻滞（P〈0.001）。同时,两种细胞的流式分析结果中均未见到细胞凋亡峰的存在,表明SAM处理并不导致细胞凋亡。结论甲基化药物SAM具有抑制结直肠癌细胞生长、阻滞细胞周期的作用,提示SAM有望成为结直肠癌治疗的新的途径。

英文摘要：

Objective To evaluate the effects of methylation agent S - adenosyl - L - methionine （SAM） on the biological behaviors of colorectal cancer （CRC） cell lines, SW620 and LoVo. Methods LoVo and SW620 were treated with SAM for 6 days. Cell proliferation and cell cycle were assessed by plate colony formation assay and flow cytometry assay, respectively. Meanwhile, the efficacy of SAM on CRC cell apoptosis was also analyzed by flow cytometry. S - adenosyl -L - homocysteine （SAH） -treated cells and mock -treated cells were used as control groups in our study. Results A significant inhibition of cell proliferation was observed in SAM -treated SW620 and LoVo cells as compared with SAH - treated cells （ P 〈 0. 001 ）. In addition, a significant reduction of the plate colony formation was also observed in SAM - treated cells as compared with SAH - treated cells and mock - treated cells （ P 〈 0. 001 ）. However, no apoptosis peak was detected in SAM -treated cells. Conclusion Methylation agent SAM can not only inhibit cell proliferation but also result in the arrest of cell cycle. Our study suggests a potential role of SAM in the clinical treatment of CRC.