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目的 探讨抗癌新药肌氨酰胺亚硝脲 (2 chloroethyl 3 sarcosinamide 1 nitrosourea ,SarCNU)在体内对DNA修复基因表达阳性肿瘤的抗肿瘤作用。方法 将人肺癌细胞株NCI H5 2 2接种于裸鼠皮下 ,制作肿瘤模型 ,观察SarCNU的抗肿瘤作用。同时 ,采用逆转录 -聚合酶链反应 (reverse transcriptionpolymerasechainreac tion ,RT PCR)测定肿瘤标本的神经元外单胺递质载体 (extraneuronalmonoaminetransporter ,EMT)和DNA修复基因六氧甲基鸟嘌呤DNA甲基转移酶 (O6 methylguanine DNAmethyltransferase ,MGMT)、核苷酸剪切修复基因ER CC1 6 (excisionrepaircross complementingrodentrepairdeficiencygene 1 6 )的表达。结果 荷瘤鼠接受SarCNU治疗后肿瘤均明显缩小 ,实验组肿瘤与对照组肿瘤大小变化 (T/C % )最佳比值为 2 3 ,肿瘤生长延缓达 5 5天 ,显示了良好的抗肿瘤作用。肿瘤细胞的EMT和DNA修复基因MGMT以及ERCC1 6的表达均为阳性。结论 在EMT阳性的肿瘤 ,即使具有DNA修复基因表达 ,SarCNU仍然具有良好的抗肿瘤作用
Objective To investigate the antitumor effect of a novel anticancer drug, chloroethyl 3 sarcosinamide 1 nitrosourea (SarCNU), on DNA repair gene-positive tumors in vivo. Methods Human lung cancer cell line NCI H5 2 2 was inoculated subcutaneously in nude mice to make a tumor model. The anti-tumor effect of SarCNU was observed. At the same time, extraneuronal monoamine transmitter (EMT) and DNA repair gene hexamethylguanine DNA methyltransferase were measured by reverse transcription polymerase chain reaction (RT PCR) in tumor samples. (O6 methylguanine DNAmethyltransferase, MGMT), nucleotide cleavage repair gene ER CC1 6 (excisionrepaircross complementing the dendrepairdeficiencygene 16) expression. Results The tumors of tumor-bearing mice were significantly reduced after SarCNU treatment. The optimal tumor ratio (T/C %) in the experimental group and the control group was 2 3, and the tumor growth was delayed for 5 5 days, indicating a good anti-tumor effect. . The expression of EMT and DNA repair genes MGMT and ERCC16 of tumor cells were positive. Conclusion SarCNU still has good anti-tumor effect in EMT-positive tumors even with DNA repair gene expression.