| Project/Area Number |
06454608
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human genetics
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| Research Institution | Medical Institute of Bioregulation, Kyushu University |
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Principal Investigator |
SASAZUKI Takehiko Medical Institute of Bioregulation, Kyushu University, Professor, 生体防御医学研究所, 教授 (50014121)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Ken Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (60274528)
FUKUI Yoshinori Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (60243961)
KAMIKAWAJI Nobuhiro Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (90224659)
TANIGUCHI Shunichiro Sinshu University, School of Medicine Professor, 医学部, 教授 (60117166)
木村 彰方 九州大学, 生体防御医学研究所, 助教授 (60161551)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 1995: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1994: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Colon cancer cell lines / homologous recombination / K-ras gene / 大腸癌細胞株 / 血管内皮増殖因子 / K-ras / P53 / 相同組み換え |
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| Research Abstract |
We have established the colon cancer cell lines in which the mutated K-ras gene was replaced by the normal K-ras gene, using homologous recombination. The comparative analyzes between these cell lines and the parental cell lines made it feasible to directly assess the role of the mutated K-ras gene in oncogenesis. As compared with the parental cell lines, the cell lines which lack the expression of the mutated K-ras gene showed the remarkable induction of C-fos and C-jun expression by the serum stimulation and the suppression of vascular endothelial growth factor (VEGF) production. These observations indicate that the mutated K-ras gene is involved in the suppression of the immediate early genes expression and the production of VEGF.Our strategy could be applied to clarify the role of the mutation in other oncogenes and tumor suppressor genes in oncogenesis.
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