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[氯化镉诱导人支气管上皮细胞转化不同阶段TIF3 p36的表达变化]

[Expression change of TIF3 p36 at different stages of human bronchial epithelial cells transformed and induced by cadmium chloride].

作者信息

Wei Lian, Lei Yi-xiong, Wang Min, Hu Bing

机构信息

Department of Preventive Medicine, Guangzhou Medical College, Guangzhou 510182, China.

出版信息

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2006 Oct;24(10):578-81.

Abstract

OBJECTIVE

To explore the molecular mechanisms potentially responsible for carcinogenesis due to cadmium by detecting expression change of the translation initiation factor 3 (TIF3 p36) in those malignant transformation of human bronchial epithelial cell lines (16HBE) induced by cadmium chloride (CdCl(2)).

METHODS

The expression changes of TIF3 p36 were detected and analyzed at different stages of malignant cells (semi transformed cells, transformed cells and tumorigenic cells) induced by CdCl(2) solution with both reverse transcription PCR technique and sensitive fluorescent quantitative PCR assay.

RESULTS

Compared with non-transformed human bronchial epithelial cells, the results of fluorescent quantitative PCR assay showed that the semi-transformed cells, transformed cells and tumorigenic cells all expressed higher levels of TIF3 p36 mRNA (P < 0.01 or P < 0.05). As compared with the control cells, the TIF3 expressions at different stages of malignant transformation were 3.1 times, 5.9 times and 9.9 times higher respectively in the low dosage group of CdCl(2) (5 micromol/L); 7.1 times, 6.8 times and 14.8 times respectively in the middle dosage group of CdCl(2) (10 micromol/L); 3.6 times, 3.0 times and 9.1 times respectively in high of dose of CdCl(2) (15 micromol/L). These results showed that there was the positive correlation between overexpression levels of TIF3 p36 mRNA and the malignant degree of the cells, but they were not related to the dosages of cadmium.

CONCLUSION

There is significantly abnormal overexpression of TIF3 gene during malignant transformation of human bronchial epithelial cell line induced by cadmium chloride, and the TIF3 expression is associated with the malignant degree of the cells, which may be one of molecular mechanisms potentially responsible for the carcinogenesis due to cadmium.

摘要

目的

通过检测氯化镉(CdCl₂)诱导人支气管上皮细胞系(16HBE)恶性转化过程中翻译起始因子3(TIF3 p36)的表达变化,探讨镉致癌可能的分子机制。

方法

采用逆转录PCR技术和灵敏的荧光定量PCR检测分析CdCl₂溶液诱导的恶性细胞(半转化细胞、转化细胞和致瘤细胞)不同阶段TIF3 p36的表达变化。

结果

荧光定量PCR检测结果显示,与未转化的人支气管上皮细胞相比,半转化细胞、转化细胞和致瘤细胞中TIF3 p36 mRNA表达均升高(P<0.01或P<0.05)。与对照细胞相比,低剂量组(5 μmol/L)CdCl₂诱导的恶性转化不同阶段TIF3表达分别升高3.1倍、5.9倍和9.9倍;中剂量组(10 μmol/L)CdCl₂诱导的分别升高7.1倍、6.8倍和14.8倍;高剂量组(15 μmol/L)CdCl₂诱导的分别升高3.6倍、3.0倍和9.1倍。结果表明TIF3 p36 mRNA过表达水平与细胞恶性程度呈正相关,但与镉剂量无关。

结论

氯化镉诱导人支气管上皮细胞系恶性转化过程中TIF3基因存在明显异常过表达,且TIF3表达与细胞恶性程度相关,这可能是镉致癌的潜在分子机制之一。

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