Open AccessExon 2 deletion splice variant of γ‐glutamyl carboxylase causes des‐γ‐carboxy prothrombin production in hepatocellular carcinoma cell lines
Author(s) -
Ueda Naoki,
Shiraha Hidenori,
Fujikawa Tatsuya,
Takaoka Nobuyuki,
Nakanishi Yutaka,
Suzuki Mayumi,
Matsuo Noriyuki,
Tanaka Shigetomi,
Nishina Shin-ichi,
Uemura Masayuki,
Takaki Akinobu,
Shiratori Yasushi,
Yamamoto Kazuhide
Publication year - 2008
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1016/j.molonc.2008.06.004
Subject(s) - exon , biology , microbiology and biotechnology , alternative splicing , cell culture , gene , splice , genetics
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.