2011 Fiscal Year Final Research Report
Investigation of chromatin remodeling by histone modifier protein in carcinogenesis and progression.
| Project/Area Number |
21590453
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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 | National Cancer Center Research Institute and Research Center for Innovative Oncology, National Cancer Center Hospital East |
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Principal Investigator |
FUJII Satoshi 独立行政法人国立がん研究センター, 臨床開発センター, 室長 (30314743)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 腫瘍 / ヒストン / クロマチン |
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| Research Abstract |
It is demonstrated that MEK-ERK1/2-Elk-1 pathway leads to EZH2 overexpression. The triple-negative and ERBB2-overexpressing subtypes of breast cancer are known to contain more rapidly proliferating breast cancer cells. The signaling pathway connected to EZH2 overexpression was associated with both aggressive subtypes of breast cancer, showing one of the clinicopathological significance of overexpression of histone modifier protein. The oncogenic role of EZH2, a histone modifier protein that is induced by oncogenic mutant RAS is also defined in pancreatic carcinogenesis, using pancreatic cancers of transgenic rats exogenously expressing human mutant RAS. That is, EZH2 was found to be a real effecter protein in the downstream of the MEK-ERK pathway in pancreatic carcinogenesis.
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