| Project/Area Number |
20590380
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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 |
Experimental pathology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KURATA Shunichi Tokyo Medical and Dental University, 難治疾患研究所, 准教授 (60140901)
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| Co-Investigator(Renkei-kenkyūsha) |
KATOH Iyoko 山梨大学, 医学工学総合研究部, 准教授 (20333297)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 細胞 / 扁平上皮癌 / p63 / SCC / EMT / invasion / Smad / IKK-α / GSK-3β / IKKα / PP2A / TGF-β / p53 |
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| Research Abstract |
To understand the functions of p63 in squamous cell carcinomas (SCC) and the malignant progression, we performed gene expression profiling after p63 silencing in cell lines. Cellular signaling mechanisms that induce p63 and block the malignant conversion were also studied. p63-knockdown cells showed loss of varied gene expression for epithelial cell adhesion and keratinocyte differentiation. Increases in gene expression associated with malignant cancers were also detected, suggesting epithelial-mesenchymal transition (EMT)-like events. Furthermore, we determined that Np63 is induced by the keratinocyte-specific TGF- signaling with IKK . The mutual induction between p63 and IKK and the transcriptional control in each system may altogether block the gain of invasive phenotype in early phase SCC.
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