BPDE诱发16HBE恶性转化过程中eIF3 p36的表达变化

目的探讨二羟环氧苯并芘（BPDE）诱发人支气管上皮细胞（16HBE）恶性转化过程中不同阶段真核生物蛋白翻译启始因子（elF3 p36 mRNA）表达水平的变化，为进一步阐明BPDE的分子致癌机理提供线索。方法应用RT—PCR和FQ—PCR方法，检测并分析BPDE诱发16HBE恶性转化不同阶段的eIF3p36mRNA表达量的变化。结果相对于非转化对照细胞，BPDE诱发恶性转化16HBE不同阶段细胞（转化细胞和成瘤细胞）的eIF3p36mR-NA基因表达水平均显著高于对照组（P〈0．01或P〈0．05），其中BPDE-转化细胞的elF3 p36平均表达量分别是对照细胞的2．3～5．1倍：而BPDE-转化细胞与BPDE-成瘤细胞的elF3 p36平均表达量相比，差别无显著性（P〉0．05），提示elF3 p36的异常表达量与BPDE诱发16HBE细胞恶变程度之间存在一定的正向关系。结论BPDE在诱发16HBE细胞恶变过程中，存在明显的elF3 p36的异常表达现象，其表达水平与细胞的恶变程度密切相关，这可能是BPDE诱发人细胞肿瘤的重要分子致癌机理之一。

Expression and changes of elF3 p36 during the malignant transformation of human bronchial epithelial cells induced by BPDE at various stages

Objective To explore the molecular mechanisms potentially responsible for careinogensis due to dihydroxyepoxybenzopyrene （BPDE） by detecting expression changes of eIF3 p36 mRNA in malignant transformation of human bronchial epithelial cell lines （16HBE） induced by BPDE. Methods The expression changes of TIF3 p36 were detected and analyzed during different stages of malignant cells （transformed cells and tumorigenic ceils） induced by CdC1a solution with both RT - PCR and FQ - PCR assays. Results Compared with non - transformed human bronchial epithelial cells , the results of FQ - PCR showed that the transformed cells and tumorigenic cells eIF3 p36 mRNA all expressed higher levels o （P 〈 0.01 or P 〈 0.05）. As compared with control cells, the eIF3 expressions during different stages of malignant transformation were higher by 2.3 to 5.1 folds. There also was no significant difference between mean expression rates of eIF3 p36 mRNA in BP- DE - transformant and that in BPDE - tumorigenic cells （ P 〉 0.05）. These results showed that there were some positive correlation （r = ？） between overexpression levels of eIF3 p36 mRNA and malignant degree of the cells. Conclusion There is markedly abnormal overexpression of eIF3 gene during malignant transformation of human bronchial epithelial cell line induced by BPDE, and the level of eIF3 expression was associated with malignant degree of the cells. It might be＇ one of the molecular mechanism potentially responsible for carcinogensis induced by BPDE.