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Carcinogenesis Advance Access originally published online on December 19, 2003
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Carcinogenesis, Vol. 25, No. 4, 483-492, April 2004
Carcinogenesis vol.25 no.4 © Oxford University Press 2004; all rights reserved.

CANCER BIOLOGY

Delayed liver regeneration and increased susceptibility to chemical hepatocarcinogenesis in transgenic mice expressing a dominant-negative mutant of connexin32 only in the liver

Maria Lúcia Zaidan Dagli1,2, Hiroshi Yamasaki1,3, Vladimir Krutovskikh1 and Yasufumi Omori1,4,5

1 Unit of Multistage Carcinogenesis, International Agency for Research on Cancer, 150, cours Albert-Thomas, 69372 Lyon Cedex 08, France
Present addresses: 2 Department of Pathology, Faculty of Veterinary Medicine and Zootechny, University of São Paulo, CEP 05508-900, S. Paulo-SP, Brazil, 3 School of Science and Technology, Kwansei Gakuin University, Sanda 669-1337, Japan and 4 Department of Pathology, Akita University School of Medicine, Akita, 010-8543, Japan

A growing body of evidence from in vitro studies indicates that gap junction proteins connexins may have a tumor-suppressor function. Our previous double transfection experiments on HeLa cells have shown that a dominant-negative mutant V139 M of connexin32 (Cx32) can abolish gap junctional intercellular communication (GJIC). To examine whether the same dominant-negative mutant of Cx32 inhibits GJIC between hepatocytes in vivo and thus modulates cell proliferation and susceptibility to hepatocarcinogenesis, we created transgenic mice with the mutant Cx32 gene driven by a liver-specific albumin promoter. These mice developed normally both before and after birth, and GJIC in their liver was diminished, as expected. No increase in incidence of spontaneous tumors of any site was observed in the transgenic mice. Rather unexpectedly, cell proliferation during liver regeneration after partial hepatectomy was retarded by 24 h in the transgenic mice compared with the wild-type mice. In contrast, the transgenic male mice were more susceptible to diethylnitrosamine-induced hepatocarcinogenesis, developing more liver tumors with shorter latency. These results show that GJIC can coordinate cell growth both positively and negatively in vivo, supporting the idea that GJIC is essential for maintenance of homeostasis.


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