目的：探讨甲基化抑制剂5-氮杂-2′-脱氧胞苷（5-Aza-2′-deoxycytidine, 5-Aza-CdR）对肿瘤细胞中NY-ESO-1抗原表达的诱导作用。方法：常规培养人胃癌细胞株SGC-7901、人肝癌细胞株H2P和MHCC97-H、人结肠癌细胞株HT-29和LoVo及人脑胶质瘤细胞株U251，RT-PCR和免疫细胞化学法检测5-Aza-CdR作用前后肿瘤细胞中NY-ESO-1 mRNA和蛋白的表达。结果：RT-PCR与免疫细胞化学检测仅见胃癌SGC-7901细胞阳性表达NY-ESO-1，其余5株肿瘤细胞不表达NY-ESO-1。NY-ESO-1阴性的肝癌细胞株H2P、结肠癌细胞株LoVo及脑胶质瘤细胞株U251经5-Aza-CdR（终浓度分别为1、5和10 μmol/L）处理6 d后，细胞形态和生长速度均无明显改变，而NY-ESO-1 mRNA和蛋白均被诱导为阳性表达，并随5-Aza-CdR浓度增加而阳性表达逐渐增强。结论：5-Aza-CdR能诱导肝癌、结肠癌、脑胶质瘤等肿瘤细胞中NY-ESO-1抗原的表达，为肿瘤免疫治疗提供了一条新思路。

Objective:To study the role of a demethylating agent, 5-Aza-2′-deoxycytidine (5-Aza-CdR),in inducing NY-ESO-1 antigen expression in tumor cells. Methods: Human gastric cancer cell line SGC-7901, hepatoma cell lines H2P and MHCC97-H, colon cancer cell lines HT-29 and LoVo, and glioma cell line U251 were used in the present study. NY-ESO-1 mRNA and protein expressions were detected by RT-PCR and immunocytochemistry in the above cell lines before and after 5-Aza-CdR treatment. Results: NY-ESO-1 antigen was positive only in gastric cancer cell line SGC-7901 as detected by RT-PCR and immunocytochemistry. The morphology and growth of hepatoma cell H2P, colon cancer cell LoVo and glioma cell U251 were not obviously affected after 5-Aza-CdR treatment (1 μmol/L, 5 μmol/L and 10 μmol/L ) for 6 days; however, 5-Aza-CdR induced NY-ESO-1 mRNA and protein expressions in these cell lines in a dose-dependent manner. Conclusion: 5-Aza-CdR can induce the expression of NY-ESO-1 antigen in hepatoma, colon cancer and glioma cells, which casts new lights on tumor immunotherapy.

福建省自然科学基金资助项目（No.C0610023），福建医科大学教授基金资助项目（No.JS08006）