Oncogenic potential of EAG K+ channels
Oncogenic potential of EAG K+ channels
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DOI：
10.1093/emboj/18.20.5540
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发表时间：
1999-10-15
期刊：
影响因子：
11.4
通讯作者：
Stühmer, W
中科院分区：
文献类型：
--
作者：
Pardo, LA;del Camino, D;Stühmer, W
我们研究了细胞周期调节的K+通道Ether a go-go（EAG）在细胞增殖和转化中的可能意义。我们表明，EAG转染到哺乳动物细胞赋予转化表型。此外，人EAG mRNA在几种体细胞癌细胞系中有缺陷，尽管在正常组织中优先在脑中表达。在几种这些癌细胞系中抑制EAG表达导致细胞增殖显著降低。此外，EAG的表达有利于肿瘤进展时，转染细胞注射到免疫抑制小鼠。这些数据为EAG的致癌潜力提供了证据。
We have investigated the possible implication of the cell cycle-regulated K+ channel ether a go-go (EAG) in cell proliferation and transformation. We show that transfection of EAG into mammalian cells confers a transformed phenotype. In addition, human EAG mRNA is defected in several somatic cancer cell lines, despite being preferentially expressed in brain among normal tissues, Inhibition of EAG expression in several of these cancer cell lines causes a significant reduction of cell proliferation. Moreover, the expression of EAG favours tumour progression when transfected cells are injected into immune-depressed mice. These data provide evidence for the oncogenic potential of EAG.