Noguchi M, Nomata K, Watanabe J, Kanetake H, Saito Y
Department of Urology, Nagasaki University School of Medicine, Japan.
Cancer Lett. 1998 Jan 9;122(1-2):77-84. doi: 10.1016/s0304-3835(97)00372-8.
Gap junctional intercellular communications (GJIC) are known as the channels for the direct transfer of cytoplasmic molecules between neighboring cells and are lost during transformation of normal cells. To study the function and the molecular mechanism for the loss of GJIC, the effects of dimethylnitrosamine, KBrO3 and FeSO4 x 7H2O, which are known as chemical tumor promoters of the kidney on the GJIC function and the expression of connexin 43 of Madin-Darby canine kidney (MDCK) epithelial cells, were examined. These tumor promoters inhibited the GJIC in MDCK cells. The expression of connexin 43 mRNA and connexin 43 protein was not altered by these treatments, whereas immunocytochemical study revealed that the distribution of connexin 43 protein was changed from the cell surface to the cytoplasma. These data suggest that blockage of GJIC in MDCK cells treated with renal carcinogens support the hypothesis that loss of GJIC might be important in renal carcinogenesis.
缝隙连接细胞间通讯（GJIC）是相邻细胞间细胞质分子直接转移的通道，在正常细胞转化过程中会丧失。为了研究GJIC丧失的功能和分子机制，检测了已知的肾脏化学肿瘤启动剂二甲基亚硝胺、溴酸钾和硫酸亚铁（FeSO4·7H2O）对Madin-Darby犬肾（MDCK）上皮细胞GJIC功能和连接蛋白43表达的影响。这些肿瘤启动剂抑制了MDCK细胞中的GJIC。这些处理并未改变连接蛋白43 mRNA和连接蛋白43蛋白的表达，而免疫细胞化学研究显示连接蛋白43蛋白的分布从细胞表面转移至细胞质。这些数据表明，用肾致癌物处理的MDCK细胞中GJIC的阻断支持了GJIC丧失可能在肾癌发生中起重要作用这一假说。
