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Leukocyte cell‐derived chemotaxin 2 (LECT2) is a potential serum biomarker specific for βcatenin mutation in hepatocellular carcinoma (144.8)
Author(s) -
Okabe Hirohisa,
Delgado Evan,
Min Lee,
Singh Sucha,
Tsung Allan,
Monga Satdarshan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.144.8
Subject(s) - hepatocellular carcinoma , biomarker , cancer research , mutation , catenin , gene , wnt signaling pathway , liver cancer , cell , cancer , medicine , biology , genetics
Objective: Molecular characteristic of tumor is currently crucial information in terms of the sensitivity to therapeutic agent and the prediction of clinical course. The aim of this study is to identify a biomarker specific for β‐Catenin gene (CTNNB1) mutation seen in 20‐30% of patients with hepatocellular carcinoma (HCC). Methods: We looked for secreted factors specific for CTNNB1 mutation using microarray analysis previously published, and validated it using stable transfectants with β‐Catenin wild‐type (Hep3BWT) and mutated form (Hep3BS33Y). Serum level of the biomarker and genetic background of primary tumor were examined in mice with liver cancer caused by diethylnitrosamine (DEN) + phenobarbital diet, which is known to induce HCC via CTNNB1 mutation. Results: Leukocyte cell‐derived chemotaxin 2 (LECT2) is downregulated in β‐Catenin KO livers. Hep3BS33Y secreted more LECT2 and showed higher promoter activity of LECT2 compared to Hep3BWT. Mice with β‐Catenin mutated (S33Y) liver cancer showed significantly higher serum LECT2 level than control or non‐tumor bearing mice. They showed high glutamine synthetase and lect2 gene expression. Conclusion: Serum LECT2 level can be a predictive biomarker for β‐Catenin activation in HCC.