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Induction of Heat Shock Gene Expression without Heat Shock by Hepatocarcinogens and during Hepatic Regeneration in Rat Liver

Departments of Medical Oncology and Therapeutics Research [B. I. C.], Molecular Genetics [T. H. H., K. I.], and Cytogenetics [C. H. B.], City of Hope National Medical Center, Duarte, California 91010

We investigated the expression of the rat hepatic heat-shock protein (hsp) genes under the influence of hepatocarcinogens and during hepatic regeneration. This was undertaken because of the inducibility of the heat-shock response in rat liver and because heat-shock genes can be expressed with or without heat shock in various cell states in a developmentally regulated manner. We found that acute administration of hepatocarcinogens to rats induced an increased hsp gene transcription in a time- and dose-dependent manner. Chronic exposure of rats to complete hepatocarcinogens induced increased levels of mainly M_r 83,000 heat-shock protein gene transcription and, to a lesser extent, M_r 70,000 heat-shock protein. However, the tumor promoter phenobarbital did not induce increased hsp gene expression. Increased levels of both M_r 83,000 heat-shock protein and M_r 70,000 heat-shock protein gene transcription were found during hepatic regeneration. Thus, increased hsp gene transcription, which correlated with increased heat-shock protein synthesis, was observed under the acute and chronic influence of hepatocarcinogens and during normal hepatic proliferation. These results are similar to those observed for c-H-ras and c-myc expression in rat liver, and they suggest that a coordinate expression of these three genes may occur in hepatic regeneration and in the early stages of experimental chemical hepatocarcinogenesis.

¹ To whom requests for reprints should be addressed, at the Department of Medical Oncology and Therapeutics Research, City of Hope National Medical Center, 1500 E. Duarte Rd., Duarte, CA 91010.

Received 4/ 9/86. Revised 6/20/86. Accepted 7/ 7/86.

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