Hypermethylation associated with inactivation of the SOCS-1 gene, a JAK/STAT inhibitor, in human hepatoblastomas

J Hum Genet. 2003;48(2):65-9. doi: 10.1007/s100380300008.

Abstract

We recently demonstrated inactivation in hepatocellular carcinomas (HCCs) of the gene encoding SOCS1/JAB1/SSI-1, a JAK-binding protein that regulates the JAK/STAT signal-transduction pathway. In a follow-up immunochemical investigation of expression of SOCS-1 in hepatoblastomas (HBLs), the protein was markedly reduced in half of the HBL tumors we examined. CpG-rich regions upstream of the SOCS-1 gene were hypermehylated in 7 of the 15 HBL cases. The results suggest that hypermethylation may play an important role in silencing the SOCS-1 gene, not only in adult HCCs, but also in liver tumors arising in childhood.

MeSH terms

  • Adolescent
  • Carrier Proteins / genetics*
  • Carrier Proteins / metabolism
  • Carrier Proteins / physiology*
  • Child
  • DNA Methylation*
  • DNA-Binding Proteins / metabolism
  • Female
  • Gene Expression
  • Gene Silencing
  • Genes, Tumor Suppressor
  • Hepatoblastoma / genetics*
  • Hepatoblastoma / metabolism
  • Hepatoblastoma / pathology
  • Humans
  • Infant
  • Intracellular Signaling Peptides and Proteins*
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • Male
  • Repressor Proteins*
  • Suppressor of Cytokine Signaling 1 Protein
  • Suppressor of Cytokine Signaling Proteins

Substances

  • Carrier Proteins
  • DNA-Binding Proteins
  • Intracellular Signaling Peptides and Proteins
  • Repressor Proteins
  • SOCS1 protein, human
  • Suppressor of Cytokine Signaling 1 Protein
  • Suppressor of Cytokine Signaling Proteins