| Project/Area Number |
24700973
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Kanazawa University |
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Principal Investigator |
SASAKI Soichiro 金沢大学, がん進展制御研究所, 博士研究員 (50583473)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ケモカイン / 大腸がん / 線維化 / HB-EGF |
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| Research Abstract |
We investigated the cellular and molecular mechanism underlying chronic inflammation-associated carcinogenesis, by using mouse colon carcinogenesis caused by azoxymethane injection combined with repeated ingestion of dextran sodium sulphate solution.
In this colon carcinogenesis process, colon tissues produced an inflammatory chemokine, CCL3, which induced fibroblasts to accumulate in and around tumor tissues and to produce a potent growth factor, heparin-binding epidermal growth factor-like growth factor (HB-EGF) in addition to the induction of inflammatory cell infiltration.
These observations would indicate that CCL3 can contribute to chronic colitis-associated carcinogenesis by regulating not only inflammatory cell infiltration but also the accumulation and functions of fibroblasts, the cells that have crucial roles in tumor microenvironment. Thus, CCL3 can be a novel molecular target for inflammation-associated carcinogenesis.
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