Exon 2 deletion splice variant of γ-glutamyl carboxylase causes des-γ-carboxy prothrombin production in hepatocellular carcinoma cell lines

Naoki Ueda, Hidenori Shiraha, Tatsuya Fujikawa, Nobuyuki Takaoka, Yutaka Nakanishi, Mayumi Suzuki, Noriyuki Matsuo, Shigetomi Tanaka, Shin ichi Nishina, Masayuki Uemura, Akinobu Takaki, Yasushi Shiratori, Kazuhide Yamamoto

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

Using GGCX gene-specific real-time PCR, exon 2 deletion splice variant of vitamin K-dependent γ-glutamyl carboxylase (GGCX) mRNA was identified in HCC cell lines. Expressions of wild type and exon 2 deletion variant of GGCX were analyzed with relevance to DCP production in HCC cell lines. Hep3B, HepG2, HuH1, HuH7, and PLC/PRF/5 produced DCP, while SK-Hep-1, HLE, HLF, and JHH1 produced no detectable level of DCP. DCP-producing cells expressed exon 2 deletion variant of GGCX mRNA and protein, while DCP-negative cells expressed no detectable level of exon 2 deletion variant of GGCX. These results suggest that exon 2 deletion splice variant of GGCX causes dysfunction of GGCX enzyme activity resulting in DCP production in HCC cell lines.

Original languageEnglish
Pages (from-to)241-249
Number of pages9
JournalMolecular Oncology
Volume2
Issue number3
DOIs
Publication statusPublished - Oct 2008

Keywords

  • Dominant-negative inhibitor
  • Prothrombin
  • Splice variant
  • Tumor markers
  • Vitamin K-dependent proteins

ASJC Scopus subject areas

  • Molecular Medicine
  • Genetics
  • Oncology
  • Cancer Research

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