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雷毅雄, 陈学敏, 陈家堃. 镉应答癌基因蛋白对细胞原癌基因表达的影响[J]. 中国公共卫生, 2004, 20(12): 1416-1417.
引用本文: 雷毅雄, 陈学敏, 陈家堃. 镉应答癌基因蛋白对细胞原癌基因表达的影响[J]. 中国公共卫生, 2004, 20(12): 1416-1417.
LEI Yi-xiong, CHEN Xue-min, CHEN Jia-kun. Effects of cadmium-responsive oncoprotein on cellar proto-oncogene gene expression[J]. Chinese Journal of Public Health, 2004, 20(12): 1416-1417.
Citation: LEI Yi-xiong, CHEN Xue-min, CHEN Jia-kun. Effects of cadmium-responsive oncoprotein on cellar proto-oncogene gene expression[J]. Chinese Journal of Public Health, 2004, 20(12): 1416-1417.

镉应答癌基因蛋白对细胞原癌基因表达的影响

Effects of cadmium-responsive oncoprotein on cellar proto-oncogene gene expression

  • 摘要:
      目的   探讨镉应答癌基因蛋白(TEF-1δ编码蛋白)对多种不同细胞肿瘤相关基因表达的影响, 以阐明镉的分子致癌机制。
      方法   应用TEF-1δ基因真核细胞稳定表达系统和Westernblot检测技术,用各种单克隆抗体检测细胞肿瘤相关基因蛋白的表达情况。
      结果   相对于载体转染中国地鼠卵巢细胞(CHO)对照细胞, 在4株具有高效稳定表达TEF-1δ编码蛋白质的CHO细胞系中均有细胞原癌基因c-fos高表达, 其编码蛋白(55kDa)含量均明显高于对照组。同样, 4株高效稳定表达TEF-1δ编码蛋白质的CHO系均具有相对较高的细胞周期调控基因Cyclin D1(编码蛋白36kDa)的表达.其余肿瘤相关基因蛋白如pan-ras, c-myc, c-jun, MDM2, ODC, p16, p53的表达在TEF-1δ转基因细胞与对照细胞之间未见明显差别。
      结论   镉应答原癌基因TEF-1δ的超额表达可调高细胞原癌基因c-fos和细胞周期调控基因Cyclin D1的表达, 这可能是镉应答原癌基因TEF-1δ的分子致癌机制。

     

    Abstract:
      Objective   To explore the molecular mechanisms potentially responsible for carcinogensis due to cadmium, the effects of cadmium-responsive oncoprotein (TEF-1δ enco ded protein) on several different genes related to cellar tumors were investigated.
      Methods   The expression of genes related to cellar tumors were detected by various monoclonal antibodies with stable transfection of mammalian cells with TEF-1δ gene and by western blot analysis.
      Results   All of the 4 different CHO cell lines stably expressed very high levels of TEF-1δ encoded protein showed over expression of cellular proto-oncogene c-fos, and the level of c-fos encoded protein(55 kDa)was very high as compared with stable-transfection of CHO cells with vector that was used as a control.All CHO cells which stably expressed very high level of TEF-1δ encoded protein demonstrated relatively high expression of cell cycle controlling gene Cyclin D1(encoded 36 kDa protein)as compared with the vector control.There were no differences between CHO cell lines stably expressed very high levels of TEF-1δ encoded protein and the vector control cells for the other oncoproteins of pan-ras, c-myc, c-jun, MDM 2, ODC, p16, p53.
      Conclusion   The translational up-regulation of cellular proto-oncogene c-fos and cell cycle controlling gene Cyclin D1 caused by over expression of the TEF-1δ, may be the molecular mechanism otentially responsible for carcinogenic potential of the novel cadmium-responsive proto-oncogen.

     

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