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目的：探讨Ｅ１Ａ基因对人肺腺癌细胞的化疗增敏作用。方法：通过脂质体介导将Ｅ１Ａ基因导入人肺腺癌细胞系Ａ－ｎｉｐ９７３，经Ｇ４１８筛选获得稳定表达Ｅ１Ａ的转染细胞（Ａｎｉｐ９７３－Ｅ１Ａ）。用不同浓度顺铂、泰素及ＶＰ１６等化疗药物处理细胞，观察Ｅ１Ａ基因对人肺腺癌细胞的化疗增敏作用。结果：Ａｎｉｐ９７３－Ｅ１Ａ细胞对顺铂、泰素的敏感性显著增加，顺铂的ＩＣ５０值减少了７倍，并且敏感性随时间的延长而增加。但对ＶＰ１６，Ｅ１Ａ基因的稳定表达在该细胞系未显示增敏作用。免疫细胞化学染色显示，Ｅ１Ａ基因抑制了ＨＥＲ－２／ｎｅｕ的表达。结论：Ｅ１Ａ基因能增加人肺腺癌细胞对顺铂、泰素等化疗药物的敏感性。该作用可能与Ｅ１Ａ基因抑制ＨＥＲ－２／ｎｅｕ的表达有关。为在恶性肿瘤治疗上化疗和基因治疗联合应用的可能性提供了实验依据。
Objective: To investigate the chemosensitization effect of E1A gene on human lung adenocarcinoma cells. Methods: E1A gene was transfected into human lung adenocarcinoma cell line A-nip973 by Lipofectamine 2000, and transfected cells stably expressing E1A (Anip973-E1A) were screened by G418. With different concentrations of cisplatin, paclitaxel and VP16 and other chemotherapy drugs to treat cells, to observe the E1A gene on human lung adenocarcinoma cell chemosensitization. Results: The sensitivity of Anip973-E1A cells to cisplatin and paclitaxel was significantly increased. The IC50 of cisplatin was reduced by 7-fold, and the sensitivity increased with time. However, stable expression of the E1A gene in VP16 did not show sensitization in this cell line. Immunocytochemical staining showed that the E1A gene inhibited the expression of HER-2 / neu. Conclusion: E1A gene can increase the sensitivity of human lung adenocarcinoma cells to chemotherapy drugs such as cisplatin and taxol. This effect may be related to the inhibition of E1A gene expression of HER-2 / neu. It provides the experimental evidence for the possibility of combined application of chemotherapy and gene therapy in the treatment of malignant tumors.