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人伸长因子-1 δ 在氯化镉诱导的人支气管上皮细胞恶性转化过程中的替代表达和序列。

Alternative expression and sequence of human elongation factor-1 delta during malignant transformation of human bronchial epithelial cells induced by cadmium chloride.

机构信息

Department of Preventive Medicine, Guangzhou Medical University, Guangzhou 510182, Guangdong, China.

出版信息

Biomed Environ Sci. 2010 Apr;23(2):151-7. doi: 10.1016/s0895-3988(10)60045-1.

Abstract

OBJECTIVE

To study the alternative expression and sequence of human elongation factor-1 delta (human EF-1 delta p31) during malignant transformation of human bronchial epithelial cells induced by cadmium chloride (CdC12) and its possible mechanism.

METHODS

Total RNA was isolated at different stages of transformed human bronchial epithelial cells (16HBE) induced by CdCl2 at a concentration of 5.0 microM. Special primers and probe for human EF-1 delta p31 were designed and expression of human EF-1 delta mRNA from different cell lines was detected with fluorescent quantitative PCR technique. EF-18 cDNA from different cell lines was purified and cloned into pMD 18-T vector followed by confirming and sequencing analysis.

RESULTS

The expressions of human EF-1 beta p31 at different stages of 16HBE cells transformed by CdCl2 was elevated (P < 0.01 or P < 0.05). Compared with their corresponding non-transformed cells, the overexpression level of EF-1 delta p31 was averagely increased 2.9 folds in Cd-pretransformed cells, 4.3 folds in Cd-transformed cells and 7.2 folds in Cd-tumorigenic cells. No change was found n the sequence of overexpressed EF-1beta p31 at different stages of 16HBE cells transformed by CdCl2.

CONCLUSION

Overexpression of human EF-1beta p31 is positively correlated with malignant transformation of 16HBE cells induced by CdC12, but is not correlated with DNA mutations.

摘要

目的

研究人延伸因子-1 德尔塔(人 EF-1 德尔塔 p31)在氯化镉(CdC12)诱导的人支气管上皮细胞恶性转化过程中的替代表达和序列及其可能的机制。

方法

在浓度为 5.0 μM 的 CdCl2 诱导下,分离不同阶段转化的人支气管上皮细胞(16HBE)的总 RNA。设计人 EF-1 德尔塔 p31 的特殊引物和探针,并用荧光定量 PCR 技术检测不同细胞系中人 EF-1 德尔塔 mRNA 的表达。从不同细胞系中纯化 EF-18 cDNA,克隆到 pMD18-T 载体中,然后进行确认和测序分析。

结果

CdCl2 诱导的 16HBE 细胞不同阶段的人 EF-1β p31 的表达升高(P<0.01 或 P<0.05)。与相应的未转化细胞相比,Cd 预转化细胞中 EF-1 德尔塔 p31 的过表达水平平均增加了 2.9 倍,Cd 转化细胞中增加了 4.3 倍,Cd 致瘤细胞中增加了 7.2 倍。在 CdCl2 诱导的 16HBE 细胞不同阶段,过表达的 EF-1β p31 序列没有变化。

结论

人 EF-1β p31 的过表达与 CdC12 诱导的 16HBE 细胞的恶性转化呈正相关,但与 DNA 突变无关。

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