| Project/Area Number |
16K21159
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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 |
Human pathology
Experimental pathology
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| Research Institution | Kobe University |
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Principal Investigator |
Koma Yuichiro 神戸大学, 医学研究科, 講師 (40714647)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 食道扁平上皮癌 / 食道上皮内腫瘍 / マクロファージ / 癌・間質相互作用 / 発癌初期段階 / GSK-3α/β / β-catenin / 腫瘍関連マクロファージ / 間接共培養 / CSF3 / G-CSF / 病理学 / 食道癌 |
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| Outline of Final Research Achievements |
We observed that infiltrating macrophages (Mφs) were upregulated in esophageal precancerous lesions. Based on these findings, we established a coculture assay using human esophageal epithelial cells (Het-1A) and human acute monocytic leukemia cells (THP-1)-derived Mφs to study the roles of Mφs in esophageal carcinogenesis. In this study, we performed cDNA microarray analysis between monocultured Het-1A and co-cultured Het-1A with THP-1-derived Mφs, and found that CSF3/G-CSF expression was upregulated in Het-1A under co-culture conditions. Het-1A was found to express G-CSF receptors. Recombinant human CSF3/G-CSF (rhCSF3/G-CSF) induced cell migration and modulated GSK-3α/β-β-catenin signaling in Het-1A. Moreover, phospho-β-catenin (Ser675) expression levels were increased, and translocation of this protein from the cytoplasm to the nucleus was induced by rhCSF3/G-CSF. These results indicate that CSF3/G-CSF signaling may contribute to early esophageal carcinogenesis.
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