二甲基亚砜对neu诱导的克隆形成能力的抑制作用与neu编码的细胞表面p185水平降低以及内源性蛋白质磷酸酪氨酸含量的变化相关。

Repression of neu-induced clonogenicity by dimethylsulfoxide correlates with decreased levels of neu-encoded cell-surface p185 and changes in phosphotyrosine content of endogenous proteins.

作者信息

Matin A, Hung M C

机构信息

Department of Tumor Biology, University of Texas, M.D. Anderson Cancer Center, Houston 77030.

出版信息

Cancer Lett. 1993 Jan 15;68(1):55-60. doi: 10.1016/0304-3835(93)90219-y.

DOI:10.1016/0304-3835(93)90219-y

Abstract

Treatment of neu-transformed fibroblasts with dimethylsulfoxide (DMSO), results in change in morphology and loss of clonogenicity. Although the total amount of neu-encoded p185 protein and mRNA remained constant after DMSO treatment, cell-surface p185 decreased by 60%, indicating that transmembrane p185 protein is not located in its physiological position. The aberrant location of p185 induced by DMSO resulted in increased tyrosine phosphorylation of p185 and concomitant decreased tyrosine phosphorylation of potential substrate proteins of p185 in the cell. However, the autophosphorylation activity of p185 in vitro was unaffected by DMSO. Thus, DMSO-induced loss of clonogenicity may be due to inappropriate location of p185, which prevents interaction between p185 and its substrates and therefore inhibits p185-mediated signal transduction pathway.

摘要

用二甲基亚砜（DMSO）处理神经转化的成纤维细胞，会导致细胞形态改变和克隆形成能力丧失。尽管在DMSO处理后，神经编码的p185蛋白和mRNA的总量保持恒定，但细胞表面的p185减少了60%，这表明跨膜p185蛋白不在其生理位置。DMSO诱导的p185异常定位导致p185的酪氨酸磷酸化增加，同时细胞中p185潜在底物蛋白的酪氨酸磷酸化减少。然而，p185在体外的自磷酸化活性不受DMSO影响。因此，DMSO诱导的克隆形成能力丧失可能是由于p185定位不当，这阻止了p185与其底物之间的相互作用，从而抑制了p185介导的信号转导通路。