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Carcinogenesis Advance Access published online on December 19, 2003
Carcinogenesis, doi:10.1093/carcin/bgh050
© 2003 by Oxford University Press
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© 2003 Oxford University Press

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 Dagli 1, Hiroshi Yamasaki 1, Vladimir Krutovskikh 1, and Yasufumi Omori 1*

1 Unit of Multistage Carcinogenesis, International Agency for Research on Cancer 150, cours Albert-Thomas 69372 Lyon Cedex 08, France

* Corresponding author. E-mail: yasu{at}med.akita-u.ac.jp.

Received 5 February 2003 ; revised 25 November 2003 ; accepted 2 December 2003

Abstract

A growing body of evidence from in vitro studies indicates that gap junction proteins connexins (Cx) may have a tumor-suppressor function. Our previous double transfection experiments on HeLa cells have shown that a dominant-negative mutant V139M of 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 hours in the transgenic mice compared with the wild-type mice. In contrast, the transgenic male mice were more susceptible to diethylnitrosamineinduced 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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