| Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Outline of Final Research Achievements |
Inactivation of p53 is frequently reported in sporadic osteosarcoma (OS) in human. In mouse, an osteoblast-specific p53-knockout line (p53f/f-Sp7/OsxCre) has the high incidence of OS, and the pathological characteristics closely resemble human OS. In this study, we found that Runx3 is markedly upregulated in OS developed in p53f/f-Sp7Cre mice (p53-null OS). Runx3-knockdown suppressed tumorigenicity of p53-null OS cells in nude mice and osteoblast-specific Runx3-knockout increased OS-free survival rate of p53f/f-Sp7Cre mice, clearly showing the oncogenic function of Runx3 in p53-dieficient osteosarcomagenesis. Runx3 was found to upregulate target genes which are known to possess oncogenic functions in the absence of p53.These results reveal a novel molecular basis of p53-deficient osteosarcomagenesis in which Runx3 is involved as an oncogene.
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