| Project/Area Number |
17510028
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental impact assessment/Environmental policy
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| Research Institution | NIPPON VETERINARY AND LIFE SCIENCE UNIVERSITY |
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Principal Investigator |
TSUCHIDA Shuichi NIPPON VETERINARY AND LIFE SCIENCE UNIVERSITY, ASSOCIATED PROFESSOR, 獣医学部, 助教授 (20217326)
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| Co-Investigator(Kenkyū-buntansha) |
HARADA Takahiko NIPPON VETERINARY AND LIFE SCIENCE UNIVERSITY, PROFESSOR, 獣医学部, 教授 (70060530)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2006: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | medaka / chemical carcinogenicity / β-catenin / SMYD3 / hepatic tumor / oncology / 肝癌モデル |
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| Research Abstract |
The aim of this study was to relate our understanding of diethylnitrosamine (DEN)-induced tumor formation to β-catenin gene mutation and SMYD3 gene activation in hepatic neoplasms of exposed medaka. There were two clones for β-catenin gene in medaka with 2352 bp and 2325 bp in open reading frame length with the homology of 95 % and 87% to the amino acid sequences estimated from human β-catenin gene, respectively. Both of the two β-catenin genes were expressed in all organs examined. The phosphorylation sites in the N-termini of β-catenin were completely conserved in medaka, which suggested that the levels of cytoplasmic β-catenin in medaka were also regulated by same degradation system in cells as human. However, mutation was not detected in the estimated phosphorylation sites in DEN-induced tumors in medaka. This study could not show the association between gene mutation in β-catenin and oncogenesis in DEN-induced liver tumors in medaka. A cloned homologous gene for medaka to human SMYD3 gene had 1314 bp in ORF with the homology of 64% to the human gene. The elevated expression of SMYD3 homologous gene was observed in DEN-induced liver tumors comparing to normal liver tissue in medaka. This result implys that SMYD3 gene expression plays a role in DEN-induced liver tumors in medaka as human liver tumors.
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