Chromatin alterations and gene function disorder in MC-29 virus-derived hepatoma

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Abstract

The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones-including processed steroid receptor-may be responsible for the lack of physiological responses to steroids in VTH. Furthermore, the increased proportion of repetitive sequences in VTH DNA may be a feature of the disorder of gene regulation in malignant cells.

Original languageEnglish
Pages (from-to)509-516
Number of pages8
JournalJournal of Toxicology and Environmental Health
Volume5
Issue number2-3
Publication statusPublished - 1979

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Viruses
Chromatin
Hepatocellular Carcinoma
Genes
Steroid Receptors
Glucocorticoids
DNA
Gene expression
Liver
Enzymes
Aryl Hydrocarbon Hydroxylases
Glucose-6-Phosphatase
Nucleic Acid Repetitive Sequences
Nucleic acids
Phosphatases
Labeling
Nucleic Acids
Glucose
Catalyst activity
Cytosol

ASJC Scopus subject areas

  • Toxicology
  • Pollution

Cite this

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title = "Chromatin alterations and gene function disorder in MC-29 virus-derived hepatoma",
abstract = "The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones-including processed steroid receptor-may be responsible for the lack of physiological responses to steroids in VTH. Furthermore, the increased proportion of repetitive sequences in VTH DNA may be a feature of the disorder of gene regulation in malignant cells.",
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AU - Kovalszky, I.

AU - Gyapay, G.

AU - Lapis, K.

AU - Suba, Z.

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AB - The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones-including processed steroid receptor-may be responsible for the lack of physiological responses to steroids in VTH. Furthermore, the increased proportion of repetitive sequences in VTH DNA may be a feature of the disorder of gene regulation in malignant cells.

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