癌变·畸变·突变 ›› 2007, Vol. 19 ›› Issue (4): 267-271.doi: 10.3969/j.issn.1004-616x.2007.04.003

• 论著 • 上一篇    下一篇

氯化镉诱发16HBE细胞恶变过程中TEF_1δ p31异常表达的研究

魏 莲 雷毅雄 王 敏 李 敏 邹晓妮   

  1. 广州医学院预防医学系, 广东 广州
  • 收稿日期:2006-10-08 修回日期:2006-12-10 出版日期:2007-07-30 发布日期:2007-07-30

Abnormal Expression of TEF_1δp31 During Stages of Human Bronchial Epithelial Cells Transform ation Induced by Cadmium Chloride

WEI Lian , LEI Yi_xiong, WANG Min, LI Min, ZOU Xiao_Ni   

  1. Department of Preventive Medicine, Guangzhou Medical College, Guangzhou
  • Received:2006-10-08 Revised:2006-12-10 Online:2007-07-30 Published:2007-07-30

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),5 μmol / 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;10 μmol/ 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;15 μmol / 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_1δ p31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。

关键词: 氯化镉(CdCl2), 人支气管上皮细胞(16HBE), 恶性转化, 翻译延伸因子TEF_1δ p31, 荧光定量PCR

Abstract: 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(CdCl2). MATERIALS AND METHODS: The changes of TEF_1δ p31 mRNA in semi_transformed cells, transformed cells and tumorigenic cells induced by CdCl2 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 CdCl2 (10 μmol/L); 1.4 times,2.9 times and 8.4 times, respectively, in high concentration of CdCl2(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 cells and concentration of CdCl2 . This may be one molecular mechanisms potentially responsible for carcinogensis caused by cadmium.

Key words: cadmium chloride(CdCl2), human bronchial epithelial cell, malignant transformation, translation elongation factor TEF_1δ p31, Taqman fluorescent quantitative PCR