Omori Y, Yamasaki H
Unit of Multistage Carcinogenesis, International Agency for Research on Cancer, Lyon, France.
Int J Cancer. 1998 Nov 9;78(4):446-53. doi: 10.1002/(sici)1097-0215(19981109)78:4<446::aid-ijc10>3.0.co;2-4.
Many lines of evidence support the hypothesis that connexins form a family of tumor-suppressor genes. Transfection of connexin43 (Cx43) into rat C6 glioma cells have revealed that Cx43 functions as a growth- and tumor-suppressor in C6 cells. In previous studies, we and others have reported that several mutant connexins can inhibit gap junctional intercellular communication (GJIC) realized by the wild type in a dominant-negative manner. We have now examined dominant-negative effects of Cx43 mutants on cell growth control exerted by wild-type Cx43 in C6 cells. When 2 Cx43 mutants (L160M and A253V) were transfected into Cx43-transfected C6 cells, they restored anchorage-independent growth capacity and reinforced the tumorigenicity of these cells, meaning that these 2 mutants can inhibit growth-suppressive function of wild-type Cx43 in a dominant-negative manner. Neither of the mutants appeared to affect phosphorylation states and subcellular localization of Cx43 proteins. Intriguingly, the mutant A253V did not suppress GJIC capacity, implying a growth-suppressive pathway mediated by Cx43 may not be related to GJIC.
多条证据支持连接蛋白构成一个肿瘤抑制基因家族的假说。将连接蛋白43(Cx43)转染到大鼠C6胶质瘤细胞中发现,Cx43在C6细胞中起到生长抑制和肿瘤抑制作用。在之前的研究中,我们和其他人报道过,几种突变型连接蛋白能够以显性负性方式抑制野生型连接蛋白实现的间隙连接细胞间通讯(GJIC)。我们现在研究了Cx43突变体对野生型Cx43在C6细胞中发挥的细胞生长控制作用的显性负性效应。当将2种Cx43突变体(L160M和A253V)转染到已转染Cx43的C6细胞中时,它们恢复了这些细胞的不依赖贴壁生长能力并增强了其致瘤性,这意味着这2种突变体能够以显性负性方式抑制野生型Cx43的生长抑制功能。这两种突变体似乎均未影响Cx43蛋白的磷酸化状态和亚细胞定位。有趣的是,突变体A253V并未抑制GJIC能力,这意味着由Cx43介导的生长抑制途径可能与GJIC无关。