摘要
背景与目的:探讨氯化镉(CdCl2)诱发人支气管上皮细胞(16HBE)恶性转化过程中不同阶段人翻译延伸因子TEF-1δ p31 mRNA表达的变化,以进一步阐明CdCl2致癌的分子机制。材料与方法:应用RT与PCR技术,以及Taqman荧光定量PCR方法,检测不同浓度CdCl2诱发16HBE恶性转化3个不同阶段细胞(转化期间细胞、转化细胞和成瘤细胞)的TEF-1δ p31 mRNA表达量的变化。结果:①相对于非转化16HBE对照细胞,CdCl2诱发恶性转化3个不同阶段细胞的TEF-1δ mRNA表达水平均显著升高(P<0.01或P<0.05),5μmol/L CdCl2处理组各阶段细胞内的TEF-1δ平均表达量分别是对照细胞的3.4、5.2和6.9倍;10μmol/L CdCl2处理组各阶段细胞内的TEF-1δ平均表达量分别是对照细胞的4.1、6.9和6.3倍;15μmol/L CdCl2处理组各阶段转化细胞内的TEF-1δ平均表达量分别是对照细胞的1.4、2.9和8.4倍。提示TEF-1δ的异常表达量与CdCl2诱发16HBE细胞恶变程度之间有正相关关系(r>0.799,P<0.01)。②16HBE细胞恶变不同阶段TEF-1δp31的异常表达水平与CdCl2的剂量相关(P=0.001)。结论:氯化镉在诱发16HBE细胞恶变过程中,存在明显的人翻译延伸因子TEF-1δ p31异常表达的现象,其表达水平与细胞恶性转化程度和CdCl2的剂量密切相关,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。
BACKGROUND ＆ AIM： To explore the molecular mechanisms potentially responsible for carcinogensis due to cadmium chloride by evaluating changes of the translation enlongation factor 1δ p31（TEF-1δ p31） expression in the malignant transformation of human bronchial epithelial cell lines（16HBE） induced by cadmium chloride（CdC12） MATERIALS AND METHODS： The changes of TEF-1δ p31 mRNA in semi-transformed cells, transformed cells and tumorigenic cells induced by CdC12 solution were assessed with both RT-PCR and Taqman fluorescent quantitative PCR assay. RESULTS：①Compared with non-transformed human bronchial epithelial cells , the fluorescent quantitative PCR assay showed that the semi-transformed cells, transformed cells and tumorigenic cells all expressed higher levels of TEF-1δ p31 mRNA（P〈0.01 or P 〈0.05） . As compared with control cells, the TEF-1δ p31 expressions during the 3 different stages of malignant transformation were 3.4 times, 5.2 times and 6.9 times, respectively, in low concentration of CDCl2（5 μmol/L）; 4.1 times, 6.9 times and 6.3 times, respectively, in moderate concentration of CdC12 （10 μmol/L）; 1.4 times, 2.9 times and 8.4 times, respectively, in high concentration of CdC12（ 15 μmol/L）. These results showed a positive correlation（r〉 0.799, P〈 0.01） between overexpression levels of TEF-1δ p31 mRNA and malignant degree of the cells, but no correlation to the concentration of cadmium. ② There was a close relationship（F = 7. 128, P = 0.001） between abnormal expression of TEF-1δ p31 in different stages of 16HBE cells induced and transformed by different concentrations of CdCl2. CONCLUSION： There was marked overexpression of TEF-1δ p31 gene during malignant transformation of human bronchial epithelial cell lines induced by cadmium chloride , and the TEF-1δ p31 expression was associated with malignant degree of the ceils and concentration of CdCl2 . This may be one molecular mechanisms potentially responsible for carcinogensis caused by cad
出处
《癌变．畸变．突变》
CAS
CSCD
2007年第4期267-271,共5页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家自然科学基金(30371195)
广东省自然科学基金(06022672)
广州市科技攻关重点项目(2003Z2-E0191/E0192)
广州市市属高校科技计划项目(1002)
广州医学院自然科学基金重点项目(2006ZR004)
