| Project/Area Number |
17390374
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyoto prefectural University of Medicine |
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Principal Investigator |
SAKAKURA Chouhei Kyoto Prefectural University of Medicine, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (10285257)
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| Co-Investigator(Kenkyū-buntansha) |
HAGIWARA Akeo Kyoto Prefectural University of Medicine, Graduate School of Medicine, Associate professor, 医学研究科, 准教授 (90198648)
OKUDA Tsukasa Kyoto Prefectural University of Medicine, Graduate School of Medicine, Associate professor, 医学研究科, 准教授 (30291587)
CHIBA Tsutomu Kyoto University, Graduate School of Medicine, professor, 医学研究科, 教授 (30188487)
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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 |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 2006: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2005: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | Gastric cancer / RUNX3 / Suppressor gene |
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| Research Abstract |
The human runt-related gene RUNX3, located on chromosome 1p36, is a major mediator of signals elicited by members of the transforming growth factor-β (TGF-β) superfamily. Here we show that 45-60% of gastric cancer cell lines and surgically resected specimens do not significantly express RUNX3 due to a combination of hemizygous deletion and hypermethylation of the RUNX3 promoter region. Tumorigenicity of gastric cancer cell lines in nude mice was inversely related to their level of AML2(RUNX3) expression, and one gastric tumor associated mutation (R122C), occurring within the conserved Runt domain completely abolished the tumor suppressive effect of RUNX3. The results suggest that a lack of RUNX3 function is causally related to the genesis and progression of human gastric cancer.
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