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目的探讨氯化镉诱发人支气管上皮细胞(16HBE)恶性转化过程中不同阶段蛋白翻译起始因子(TIF3)p36mRNA表达水平的变化,为进一步阐明氯化镉的分子致癌机制提供线索。方法应用逆转录-聚合酶链式反应(RT-PCR)技术,以及敏感先进的Taqman荧光定量PCR方法,检测并分析氯化镉诱发16HBE恶性转化不同阶段即转化期间细胞、转化细胞和成瘤细胞的TIF3 p36 mRNA表达量的变化。结果相对于非转化对照细胞(16HBE),氯化镉诱发恶性转化不同阶段细胞(转化期间细胞、转化细胞和成瘤细胞)的TIF3 p36 mRNA基因表达水平均明显升高(P＜0．01或P＜0．05),其中低剂量组(5μmol/L)所转化的各阶段细胞的eIF3 p36 mRNA平均表达量分别是对照细胞的3．1、5．9和9．9倍,中剂量组(10μmol/L)的各阶段转化细胞的TIF3平均表达量分别是对照细胞的7．1、6．8和14．8倍,高剂量组(15μmol/L)的各阶段转化细胞的TIF3 p36平均表达量分别是对照细胞的3．6、3．0和9．1倍。这些不同剂量组的研究结果提示,eIF3 p36的异常表达量与氯化镉诱发16HBE细胞恶变程度之间有正相关关系,但与镉的剂量无关。结论氯化镉在诱发16HBE细胞恶变过程中,存在明显的蛋白翻译启动因子eIF3 p36异常表达现象,其表达水平与细胞的恶变程度密切相关,这可能是氯化镉诱发人细胞肿瘤的重要分子致癌机制之一。
Objective To investigate the expression of p36 mRNA in different stages of cadmium chloride-induced malignant transformation of human bronchial epithelial cells (16HBE), and to provide clues for further elucidating the molecular mechanisms of cadmium chloride. Methods Reverse transcription polymerase chain reaction (RT-PCR) and sensitive Taqman real-time PCR were used to detect and analyze the different stages of malignant transformation of 16HBE induced by cadmium chloride, ie, cells, transformed cells and tumorigenic cells Of TIF3 p36 mRNA expression changes. Results Compared with non-transformed control cells (16HBE), the expression of TIF3 p36 mRNA in different stages of cadmium chloride-induced malignant transformation of cells (transformed cells, transformed cells and tumorigenic cells) were significantly increased (P <0.01 or P <0.05). The average expression levels of eIF3 p36 mRNA in all stages of cells transformed with low dose (5μmol / L) were 3.1, 5.9 and 9.9 times that of control cells, (10μmol / L), the average expression of TIF3 in the transformed cells was 7.1, 6.8 and 14.8 times that of the control cells respectively. The average TIF3 p36 of the transformed cells in the high dose group (15μmol / L) The expression levels were 3.6, 3.0 and 9.1 times that of the control cells, respectively. The results of these different dose groups suggest that there is a positive correlation between the abnormal expression of eIF3 p36 and the malignancy of 16HBE cells induced by cadmium chloride, but not with the dose of cadmium. Conclusion Cadmium chloride (CdCl2) can induce abnormal expression of eIF3 p36 in 16HBE cells. The expression level of eIF3 p36 is closely related to the degree of cell malignant transformation induced by cadmium chloride. This may be due to the carcinogenesis of cadmium chloride One of the mechanisms.