Gap junctional intercellular communication and cell proliferation during rat liver carcinogenesis.
During multistage liver carcinogenesis, there is a sequential decrease in gap junctional intercellular communication (GJIC), associated with reduced expression of a major liver gap-junction protein (connexin 32). There are also several lines of evidence indicating that the induction of cell proliferation plays an important role during liver carcinogenesis. The relationship between GJIC and cell proliferation and their roles in liver carcinogenesis are not yet known. Results from various experiments suggest that there is a close relationship between the inhibition of GJIC and stimulation of liver cell proliferation. However, our results also suggest that different stimuli may affect cell proliferation and GJIC differentially by different mechanisms.
International Agency for Research on Cancer, Lyon, France.
H
H
Yamasaki
V
V
Krutovskikh
M
M
Mesnil
A
A
Columbano
H
H
Tsuda
N
N
Ito
D000818:Animals; D002450:Cell Communication / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D003043:Cocarcinogenesis; D017630:Connexins / Q000378:metabolism; D017629:Gap Junctions / Q000502:physiology*; D066298:In Vitro Techniques; D008114:Liver Neoplasms, Experimental / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D008115:Liver Regeneration / Q000502:physiology; D051381:Rats; D000097002:Gap Junction beta-1 Protein
D017630:Connexins; D000097002:Gap Junction beta-1 Protein