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Carcinogenesis Advance Access published online on August 14, 2003
Carcinogenesis, doi:10.1093/carcin/bgg135
© 2003 by Oxford University Press
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© 2003 Oxford University Press

CANCER BIOLOGY

Gap junctional intercellular communication and cellular response to heat stress

Nobuyuki Hamada 1, Seiji Kodama 1, Keiji Suzuki 1, and Masami Watanabe 1*

1 Division of Radiation Biology, Department of Radiology and Radiation Biology, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan

* Corresponding author. E-mail: nabe{at}net.nagasaki-u.ac.jp.

Received 20 March 2003 ; revised 25 June 2003 ; accepted 25 July 2003

Abstract

Gap junctional intercellular communication (GJIC) is essential in the maintenance of tissue homeostasis, and has been implicated in tumor suppression. Recent studies have indicated that GJIC is also involved in cellular stress responses to low-dose ionizing radiation, ultraviolet light, and hydrogen peroxide. However, the contribution of GJIC in heat stress response has not yet been elucidated. We demonstrated here a potential link between GJIC and heat stress response. First, we investigated whether the abolishment of GJIC by lindane affects heat sensitivity in normal human cells. Lindane potentiated cell killing by heat shock at 43°C, whereas little or no cytotoxicity was observed at 37°C. Nuclear translocation of heat shock protein 72 (HSP72) was interrupted by lindane, although its induction was not affected. These results indicate that lindane exacerbates hyperthermic lethality via disrupted nuclear translocation of HSP72 proteins. Second, we assessed whether heat shock alters GJIC and phosphorylation of gap junction protein connexin (Cx) in normal human cells. Persistent heat treatment augmented Cx43 phosphorylation in a heat-time-dependent fashion, and this phosphorylation was recovered after heat shock. GJIC was also disturbed by heat shock. These results indicate that heat shock augments Cx43 phosphorylation leading to GJIC abrogation. Our present results imply that GJIC contributes to the protection against heat stress, and that loss of GJIC function during carcinogenesis exacerbates hyperthermic lethality.


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