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大鼠膀胱癌发生过程中缝隙连接细胞间通讯能力增强及连接蛋白43和26表达增加。

Increased gap junctional intercellular communication capacity and connexin 43 and 26 expression in rat bladder carcinogenesis.

作者信息

Asamoto M, Takahashi S, Imaida K, Shirai T, Fukushima S

机构信息

First Department of Pathology, Nagoya City University Medical School, Japan.

出版信息

Carcinogenesis. 1994 Oct;15(10):2163-6. doi: 10.1093/carcin/15.10.2163.

Abstract

Many reports have suggested that gap junctional intercellular communication or gap junction proteins (connexins) could have tumor suppression characteristics. We investigated gap junctional intercellular communication capacity and connexin 26, 32 and 43 mRNA expression in four rat bladder cell lines and the results were compared to their tumorigenicity. We also examined connexin expression in rat bladder carcinomas induced by 3,2'-dimethyl-4-aminobiphenyl or N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN) and in normal bladders. There was clear tendency that cell lines with greater communication had stronger tumorigenicity and more expression of connexin 26 or 43. We could not detect connexin 32 in these cell lines. In normal bladder tissue, connexin 43 expression was barely detectable and there was no detectable connexin 26. However, in rat bladder carcinomas, especially the EHBN-induced carcinomas, abundant expression of both connexins was observed. These results indicate that increased gap junctional intercellular communication capacity or increased connexin(s) expression may give a growth advantage in rat bladder carcinogenesis.

摘要

许多报告表明,间隙连接细胞间通讯或间隙连接蛋白(连接蛋白)可能具有肿瘤抑制特性。我们研究了四种大鼠膀胱细胞系中的间隙连接细胞间通讯能力以及连接蛋白26、32和43的mRNA表达,并将结果与其致瘤性进行了比较。我们还检测了由3,2'-二甲基-4-氨基联苯或N-乙基-N-(4-羟基丁基)亚硝胺(EHBN)诱导的大鼠膀胱癌以及正常膀胱中的连接蛋白表达。明显的趋势是,通讯能力较强的细胞系具有更强的致瘤性,且连接蛋白26或43的表达更多。我们在这些细胞系中未检测到连接蛋白32。在正常膀胱组织中,几乎检测不到连接蛋白43的表达,也未检测到连接蛋白26。然而,在大鼠膀胱癌中,尤其是EHBN诱导的癌,观察到这两种连接蛋白均有丰富表达。这些结果表明,间隙连接细胞间通讯能力的增强或连接蛋白表达的增加可能在大鼠膀胱癌发生过程中赋予生长优势。

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