经醋酸镍（II）处理的中国仓鼠卵巢细胞差异表达波形蛋白、hSNF2H同源物和H铁蛋白。

Nickel(II) acetate-treated Chinese hamster ovary cells differentially express Vimentin, hSNF2H homologue, and H ferritin.

作者信息

Lee S H, Shiao Y H, Plisov S Y, Kasprzak K S

机构信息

Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland, 21702, USA.

出版信息

Biochem Biophys Res Commun. 1999 May 19;258(3):592-5. doi: 10.1006/bbrc.1999.0692.

DOI:10.1006/bbrc.1999.0692

PMID:10329430

Abstract

In probing the possible non-genotoxic molecular mechanism(s) of nickel(II)-induced carcinogenesis, we performed a non-radioactive mRNA differential display analysis for nickel(II) acetate-treated Chinese hamster ovary cells (CHO-K1-BH4). Three out of thirty differentially expressed cDNAs had sequences highly similar to known genes. Down-regulation of vimentin and a hSNF2H homologue and up-regulation of ferritin heavy chain were confirmed by Northern blot analysis. The expression of these mRNAs was time- and nickel(II) concentration-dependent. For vimentin, the decrease in mRNA level was concurrent with a decrease in the protein level. For ferritin, the increase in mRNA had no effect on the protein level. Dysregulation of these gene products signifies their involvement in the epigenetic effects of carcinogenic nickel(II) compounds.

摘要

在探究镍（II）诱导致癌作用的可能非遗传毒性分子机制时，我们对醋酸镍处理的中国仓鼠卵巢细胞（CHO-K1-BH4）进行了非放射性mRNA差异显示分析。30个差异表达的cDNA中有3个的序列与已知基因高度相似。通过Northern印迹分析证实了波形蛋白和一种hSNF2H同源物的下调以及铁蛋白重链的上调。这些mRNA的表达呈时间和镍（II）浓度依赖性。对于波形蛋白，mRNA水平的降低与蛋白质水平的降低同时发生。对于铁蛋白，mRNA的增加对蛋白质水平没有影响。这些基因产物的失调表明它们参与了致癌性镍（II）化合物的表观遗传效应。