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首页> 外文期刊>Cell communication & adhesion >Connexin Expression and Cell Coupling Fail to Reverse the v-src Transformed Growth Characteristics of a Cx43–/– Cell
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Connexin Expression and Cell Coupling Fail to Reverse the v-src Transformed Growth Characteristics of a Cx43–/– Cell

机译：连接蛋白表达和细胞偶联未能逆转Cx43 – / –细胞的v-src转化生长特性

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摘要

Gap junctions, composed of connexins, have been shown to suppress transformation in a variety of malignancies and transformed cell types. In addition, transforming factors such as the src oncogene have been shown to directly phosphorylate some connexins (e.g., Cx43) and inhibit coupling. To investigate the role of gap junctions in cell transformsation by v-src , we utilized a clonal cell line derived from Cx43 knockout mice (KoA) that was immortalized, but not transformed. Transfection by v-src induced a marked transformed phenotype characterized by growth in low serum and anchorage-independent conditions. Subsequent transfections by Cx43, Cx32 or vector alone were then tested for their effects on growth. Activity of pp60 v - src was confirmed in all transfectants as well as the ability of pp60 v - src to phosphorylate Cx43 in several clones. Despite the documented effect of pp60 v - src on Cx43 channel closure, modest coupling was still retained in many of the Cx43 and Cx32 transfectants. However, none of the four Cx43 transfected clones showed significant inhibitory effects on proliferation in either anchorage-independent or low serum growth conditions. Of the Cx32 clones, only one in five showed effects on growth in both assays, which was the same ratio observed for the control transfectants. Thus, based on the levels of expression achieved, which were comparable to endogenous levels in established cell lines, neither Cx43 nor Cx32 serve as effective suppressors of the transformed growth phenotype of this v-src expressing cell line.
机译：由连接蛋白组成的间隙连接已显示可抑制多种恶性肿瘤和转化细胞类型的转化。另外，已经表明转化因子例如src癌基因直接磷酸化一些连接蛋白（例如Cx43）并抑制偶联。为了研究间隙连接在通过v-src进行的细胞转化中的作用，我们利用了源于Cx43敲除小鼠（KoA）的永生化但未转化的克隆细胞系。通过v-src转染诱导了明显的转化表型，其特征是在低血清和锚定非依赖性条件下生长。然后测试单独通过Cx43，Cx32或载体进行的后续转染对生长的影响。在所有转染子中均证实了pp60 v-src的活性以及在几个克隆中pp60 v-src磷酸化Cx43的能力。尽管有文献报道pp60 v-src对Cx43通道的关闭有影响，但许多Cx43和Cx32转染子仍保留了适度的偶联。然而，在不依赖锚定或低血清生长的条件下，四个Cx43转染的克隆均未显示出对增殖的显着抑制作用。在Cx32克隆中，只有五分之一的样本在两种测定中均显示出对生长的影响，这与对照转染子观察到的比率相同。因此，基于所达到的表达水平，其与已建立的细胞系中的内源水平相当，Cx43和Cx32均不能用作该v-src表达细胞系的转化生长表型的有效抑制剂。

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