| Project/Area Number |
15K18406
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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, 助教 (50583473)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 大腸がん / CCR5 / マラビロック / 線維芽細胞 |
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| Outline of Final Research Achievements |
We previously demonstrated that locally-produced CCL3 induce the intra-tumoral accumulation of cancer-associated fibroblast (CAFs), which express CCR5, a specific receptor for CCL3. Based on these observations, we examined the effect of a CCR5 antagonist, maraviroc, on tumor growth arising from intra-cecal injection of either a mouse or a human colon cancer cell line. Oral administration of maraviroc after tumor injection decreased tumor sizes with reductions in numbers of CAFs and epidermal growth factor (EGF) expression by CAFs, but with few effects on leukocyte infiltration. Consistently, CCL3 in vitro induced fibroblasts to migrate and to express EGF, and maraviroc reduced these in vitro effects of CCL3 on fibroblasts. These observations would indicate the potential of maraviroc or other CCR5 inhibitors as a novel therapeutic modality for colon cancer, by targeting the CCL3-CCR5 interaction.
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