Igf-1 and its isoform expression in hepatic cell tumors and the surrounding tissue in mice liver carcinogenesis induced by diethylnitrozamine

The expression of the Igf-1 gene in mouse liver at different stages of development of hepatocellular carcinoma induced by diethylnitrozamine—from the initial diffuse tissue dysplasia and nodular hyperplasia to the development of multiple adenomas and carcinoma—has been analyzed. It was marked that t...

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Bibliographic Details
Published in:Biology bulletin of the Russian Academy of Sciences 2013-11, Vol.40 (6), p.519-526
Main Authors: Zinevich, L. S, Goncharova, N. O, Uryvaeva, I. V, Delone, G. V, Mikaelyan, A. S
Format: Article
Language:English
Subjects:
Biochemistry
Biomedical and Life Sciences
carcinogenesis
carcinoma
Cell Biology
developmental stages
Ecology
genes
Genetics
hepatoma
hyperplasia
Life Sciences
liver
messenger RNA
mice
Zoology
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Summary:The expression of the Igf-1 gene in mouse liver at different stages of development of hepatocellular carcinoma induced by diethylnitrozamine—from the initial diffuse tissue dysplasia and nodular hyperplasia to the development of multiple adenomas and carcinoma—has been analyzed. It was marked that the level of Igf-1 expression in all liver neoplasms decreased; it increased only in the liver tissue surrounding the carcinoma. The dependence of Igf-1 expression on inflammatory processes accompanying tumor growth was analyzed on the model of acute liver damage by diethylnitrozamine. It was established that the level of Igf-1 expression in liver tissue under acute damage in sexually mature mice was the same as in the control group. By the means of semiquantitative evaluation of the products of two Igf-1 splice isoforms—locally active (Mgf) and circulating (Igf-1v4)—it has been shown that the amount of mRNA of both isoforms in hepatocellular carcinoma was lower, and in tissue surrounding the tumor higher, than in the samples of the control group. At the same time, the proportion of transcripts of isoforms was stable.
ISSN:1062-3590
1608-3059
DOI:10.1134/S1062359013060150