Expression of c-myc promoter binding protein (MBP-1), a novel eukaryotic repressor gene, in cirrhosis and human hepatocellular carcinoma

X. Fan, H. Solomon, Kathleen Schwarz, M. C. Kew, R. B. Ray, A. M. Di Bisceglie

Research output: Contribution to journalArticle

Abstract

We have examined the expression of c-myc and c-myc promoter binding protein (MBP-1), a novel eukaryotic repressor, in human hepatocellular carcinoma and cirrhosis by semiquantitative reverse transcription PCR amplification. Levels were normalized for glyceraldehyde-3-phosphate dehydrogenase messenger RNA and then compared between these two groups and to normal liver. We found that MBP-1 expression was significantly decreased in cirrhosis and c-myc and MBP-1 were even further diminished in hepatocellular carcinoma. There was no clear correlation between MBP-1 and c-myc messenger RNA levels. Our results therefore suggest that expression of MBP-1 and c-myc are decreased in a stepwise fashion in the presence of chronic liver disease and hepatocellular carcinoma in humans and that further study of the interactions of these two genes and their products is warranted to determine their role in human hepatocarcinogenesis.

Original languageEnglish (US)
Pages (from-to)563-566
Number of pages4
JournalDigestive Diseases and Sciences
Volume46
Issue number3
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Hepatocellular Carcinoma
Carrier Proteins
Fibrosis
Genes
Messenger RNA
Glyceraldehyde-3-Phosphate Dehydrogenases
Reverse Transcription
Liver Diseases
Chronic Disease
Polymerase Chain Reaction
Liver

Keywords

  • Binding-protein
  • c-myc
  • Liver cancer
  • Oncogene

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Expression of c-myc promoter binding protein (MBP-1), a novel eukaryotic repressor gene, in cirrhosis and human hepatocellular carcinoma. / Fan, X.; Solomon, H.; Schwarz, Kathleen; Kew, M. C.; Ray, R. B.; Di Bisceglie, A. M.

In: Digestive Diseases and Sciences, Vol. 46, No. 3, 2001, p. 563-566.

Research output: Contribution to journalArticle

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