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首页> 外文期刊>Cell communication & adhesion >Maintaining Connexin43 Gap Junctional Communication in v-Src Cells Does Not Alter Growth Properties Associated with the Transformed Phenotype
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Maintaining Connexin43 Gap Junctional Communication in v-Src Cells Does Not Alter Growth Properties Associated with the Transformed Phenotype

机译：在v-Src细胞中维持Connexin43间隙连接通讯不会改变与转化表型相关的生长特性

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摘要

Loss of connexin expression and/or gap junctional communication (GJC) has been correlated with increased rates of cell growth in tumor cells compared to their normal communication-competent counterparts. Conversely, reduced rates of cell growth have been observed in tumor cells that are induced to express exogenous connexins and re-establish GJC, It is not clear how this putative growth-suppressive effect of the connexin proteins is mediated and some data has suggested that this function may be independent of GJC. In mammalian cells that express v-Src, connexin43 (Cx43) is phosphorylated on Tyr247 and Tyr265 and this results in a dramatic disruption of GJC. Cells that express a Cx43 mutant with phenylalanine mutations at these tyrosine sites form functional gap junctions that, unlike junctions formed by wild type Cx43, remain functional in cells that co-express v-Src. These cells still appear transformed; however, it is not known whether their ability to maintain GJC prevents the loss of growth restraints that confine "normal" cells, such as the inability to grow in an anchorage-independent manner or to form foci. In these studies, we have examined some of the growth properties of cells with Cx43 gap junctions that remain communication-competent in the presence of the co-expressed v-Src oncoprotein.
机译：与正常通讯能力的对应物相比，连接蛋白表达和/或间隙连接通讯（GJC）的丧失与肿瘤细胞中细胞生长速率的增加有关。相反，在诱导表达外源连接蛋白并重建GJC的肿瘤细胞中，观察到细胞生长速率降低。目前尚不清楚如何介导连接蛋白的这种假定的生长抑制作用，并且一些数据表明这一点。功能可能独立于GJC。在表达v-Src的哺乳动物细胞中，连接蛋白43（Cx43）在Tyr247和Tyr265上被磷酸化，这会导致GJC的急剧破坏。表达在这些酪氨酸位点具有苯丙氨酸突变的Cx43突变体的细胞形成功能性缺口连接，与野生型Cx43形成的连接不同，该缺口在共同表达v-Src的细胞中保持功能。这些细胞仍然看起来已经转化。但是，尚不知道它们维持GJC的能力是否会阻止限制“正常”细胞的生长限制的丧失，例如无法以不依赖锚定的方式生长或形成灶。在这些研究中，我们检查了具有Cx43间隙连接的细胞的某些生长特性，这些细胞在共表达的v-Src癌蛋白存在下仍保持通讯能力。

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