scholarly journals Gap Junctional Intercellular Communication and Cell Proliferation during Rat Liver Carcinogenesis

1993 ◽  
Vol 101 ◽  
pp. 191 ◽  
Author(s):  
Hiroshi Yamasaki ◽  
Vladimir Krutovskikh ◽  
Marc Mesnil ◽  
Amadeo Columbano ◽  
Hiroyuki Tsuda ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Rat Liver ◽  
Intercellular Communication ◽  
Gap Junctional Intercellular Communication ◽  
Liver Carcinogenesis ◽  
Gap Junctional

scholarly journals Gap junctional intercellular communication and cell proliferation during rat liver carcinogenesis.

1993 ◽  
Vol 101 (suppl 5) ◽  
pp. 191-197 ◽  
Author(s):  
H Yamasaki ◽  
V Krutovskikh ◽  
M Mesnil ◽  
A Columbano ◽  
H Tsuda ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Rat Liver ◽  
Intercellular Communication ◽  
Gap Junctional Intercellular Communication ◽  
Liver Carcinogenesis ◽  
Gap Junctional

Doxorubicin induces EGF receptor-dependent downregulation of gap junctional intercellular communication in rat liver epithelial cells

2005 ◽  
Vol 386 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Kotb Abdelmohsen ◽  
Claudia von Montfort ◽  
Dominik Stuhlmann ◽  
P. Arne Gerber ◽  
Ulrich K.M. Decking ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Rat Liver ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Egf Receptor ◽  
Gap Junctional Intercellular Communication ◽  
Erk Activation ◽  
Liver Epithelial Cells ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

Abstract Exposure of rat liver epithelial cells to doxorubicin, an anthraquinone derivative widely employed in cancer chemotherapy, led to a dose-dependent decrease in gap junctional intercellular communication (GJC). Gap junctions are clusters of inter-cellular channels consisting of connexins, the major connexin in the cells used being connexin-43 (Cx43). Doxorubicin-induced loss of GJC was mediated by activation of extracellular signal-regulated kinase (ERK)-1 and ERK-2, as demonstrated using inhibitors of ERK activation. Furthermore, activation of the epidermal growth factor (EGF) receptor by doxorubicin was responsible for ERK activation and the subsequent attenuation of GJC. Inhibition of GJC, however, was not by direct phosphorylation of Cx43 by ERK-1/2, whereas menadione, a 1,4-naphthoquinone derivative that was previously demonstrated to activate the same EGF receptor-dependent pathway as doxorubicin, resulting in downregulation of GJC, caused strong phos-phorylation of Cx43 at serines 279 and 282. Thus, ERK-dependent downregulation of GJC upon exposure to quinones may occur both by direct phosphorylation of Cx43 and in a phosphorylation-independent manner.

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