Expression of liver-enriched nuclear factors and their isoforms in alpha-fetoprotein-producing gastric carcinoma cells

Y Supriatna, T Kishimoto, M Furuya, N Tochigi, H Ishiguro, D Tosh, H Ishikura

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Alpha-fetoprotein (AFP)-producing gastric cancer (AFP-GC) is a highly malignant variant of adenocarcinoma with aberrant hepatocellular phenotype. A detailed understanding of the regulation of its liver phenotype is lacking. Liver-enriched nuclear factors (LENFs) are implicated in the transcriptional regulation of AFP in the fetal liver. To investigate the regulatory role of LENFs in AFP-GCs, the expression of LENFs including CCAAT/enhancer binding protein (C/EBP)-beta, C/EBP-alpha, hepatocyte nuclear factor (HNF)-1 alpha, HNF-1 beta and HNF-4 alpha was investigated in 3 cell lines of AFP-GC and 7 cell lines of control GC. The liver activating protein (LAP), an activating isoform of C/EBP-beta, was predominantly expressed in AFP-GCs, whereas the liver inhibitory protein (LIP), an inhibitory isoform of C/EBP-beta, predominated in the control GCs. HNF-1 alpha was relatively suppressed in AFP-GCs. HNF-4a was expressed in one of three AFP-GC cell lines. C/EBP-alpha and HNF-1 beta were expressed at the same levels in both cell types of GC. AFP-GCs expressed a set of hepatocyte-related proteins (e.g., transferrin and albumin) while they still retained the several glandular cell-related proteins (e.g., MUC2). The induction of LIP reduced transferrin expression and induced CEA expression in an AFP-GC line. Collecting these results, it was suggested that the contribution of LENFs, especially isoforms of C/EBP-beta, is possibly important in phenotypic regulation of AFP-GCs.
Original languageEnglish
Pages (from-to)316-321
Number of pages6
JournalExperimental and Molecular Pathology
Volume82
Issue number3
DOIs
Publication statusPublished - Jun 2007

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