Exon 2 deletion splice variant of γ-glutamyl carboxylase causes des-γ-carboxy prothrombin production in hepatocellular carcinoma cell lines
| Autor: | Mayumi Suzuki, Yutaka Nakanishi, Akinobu Takaki, Masayuki Uemura, Noriyuki Matsuo, Nobuyuki Takaoka, Yasushi Shiratori, Shigetomi Tanaka, Naoki Ueda, Hidenori Shiraha, Kazuhide Yamamoto, Shin Ichi Nishina, Tatsuya Fujikawa |
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| Rok vydání: | 2008 |
| Předmět: |
Cancer Research
Carcinoma Hepatocellular Exonic splicing enhancer Biology Polymerase Chain Reaction Exon Cell Line Tumor Genetics Humans RNA Messenger Protein Precursors Messenger RNA Alternative splicing Wild type Genetic Variation Exons General Medicine Molecular biology digestive system diseases Isoenzymes Real-time polymerase chain reaction Carbon-Carbon Ligases Oncology Cell culture Papers Molecular Medicine Prothrombin Vitamin K epoxide reductase Biomarkers |
| Zdroj: | Molecular Oncology. 2:241-249 |
| ISSN: | 1574-7891 |
| DOI: | 10.1016/j.molonc.2008.06.004 |
| Popis: | Using GGCX gene-specific real-time PCR, exon 2 deletion splice variant of vitamin K-dependent gamma-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. |
| Databáze: | OpenAIRE |
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