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首页> 外文期刊>Journal of biochemical and molecular toxicology >Correlation between the activation of Neu tyrosine kinase and promotion of foci formation induced by selected organochlorine compounds in the MCF-7 model system.
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Correlation between the activation of Neu tyrosine kinase and promotion of foci formation induced by selected organochlorine compounds in the MCF-7 model system.

机译：在MCF-7模型系统中，Neu酪氨酸激酶的活化与所选有机氯化合物诱导的灶形成促进之间的相关性。

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Several studies have shown that some organochlorine compounds act like estrogen in certain animals and in vitro cell culture systems, and therefore, there is a possibility that they could promote the process of tumorigenesis in breast cancer cells. In our previous study, two representative organochlorines, 1,1,1-trichloro 2-o-chlorophenyl-2'-p-chlorophenyl ethane (o,p'-DDT) and beta-1,2,3,4,5,6-hexachlorocyclohexane (beta HCH), were found to directly activate the protein tyrosine kinase of Neu (c-erbB-2 proto-oncogene product) immunoprecipitates isolated from MCF-7 breast cancer cells. In the current study, we also found that 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) at 1 nM and alpha-HCH isomers at 100 nM could also significantly activate protein tyrosine kinase of Neu immunoprecipitates in a cell-free system. We also found that organochlorines result in an increase of Neu protein tyrosine kinase after intact cell treatment in estrogen-depleted medium. This Neu kinase activation by beta-HCH (100 nM) was blocked when the cells were pretreated with Neu mRNA antisense oligonucleotide (p < 0.07, Student's t-test). Endogenously added alpha-, beta-, and gamma-HCH, o,p'-DDT, 2,2'-dichlorobiphenyl (2,2'-PCB), and 2,4,5-T at 100 nM were found to promote foci formation in postconfluent cultures of this cell line. This stimulatory effect caused by 17beta-estradiol, o,p'-DDT, and beta-HCH on foci formation was inhibited by coincubation with Neu monoclonal antibody (p < 0.05). Those two events induced by organochlorines (i.e., Neu kinase activation and foci formation) seemed causally correlated.
机译：多项研究表明，某些有机氯化合物在某些动物和体外细胞培养系统中的作用类似于雌激素，因此，它们有可能促进乳腺癌细胞的肿瘤发生过程。在我们之前的研究中，有两种代表性的有机氯：1,1,1-三氯2-邻氯苯基-2'-对氯苯基乙烷（o，p'-DDT）和β-1,2,3,4,5，发现6-六氯环己烷（βHCH）可以直接激活从MCF-7乳腺癌细胞中分离出来的Neu（c-erbB-2原癌基因产物）免疫沉淀蛋白酪氨酸激酶。在本研究中，我们还发现1 nM的2,4,5-三氯苯氧基乙酸（2,4,5-T）和100 nM的α-HCH异构体也可以显着激活细胞中Neu免疫沉淀的蛋白酪氨酸激酶-免费系统。我们还发现，在雌激素耗尽的培养基中完整细胞处理后，有机氯会导致Neu蛋白酪氨酸激酶的增加。当用Neu mRNA反义寡核苷酸预处理细胞时，β-HCH（100 nM）对Neu激酶的激活被阻断（p <0.07，Student's t检验）。发现内源添加的α-，β-和gamma-HCH，o，p'-DDT，2,2'-二氯联苯（2,2'-PCB）和2,4,5-T在100 nM时可促进此细胞系汇合后培养中的病灶形成。与Neu单克隆抗体共孵育抑制了17β-雌二醇，o，p'-DDT和β-HCH对灶形成的刺激作用（p <0.05）。有机氯诱导的这两个事件（即Neu激酶激活和病灶形成）似乎是因果相关的。

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