2006 Fiscal Year Final Research Report Summary
Cancer stem cell analysis of pancreas duct cell carcinoma a fundamental study for new strategy against pancreatic cancer
| Project/Area Number |
17591453
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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 |
Digestive surgery
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| Research Institution | Chiba Cancer Center Research Institute |
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Principal Investigator |
ASANO Takehide Chiba Cancer Center (Institute), Digestive Surgery, Director medical, 消化器外科, 診療部長 (80143311)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Cancer / Development / Differentiation / Cancer stem cell / Metastasis / Recurrence / Pancreas / pancreatic duct cell carcinoma |
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| Research Abstract |
The stem cell nitch of pancreas and the role of cancer stem cells of pancreatic carcinogenesis has been elusive. We investigate the dedifferentiation ability of mouse derived pancreatic epithelial cells under stimulation of growth factors. We observed formation of cells with a mesenchymal phenotype in murine pancreatic explants cultured on gelatin-coated dishes in the presence of serum and/or growth factors; we refer to these cells as mAPCs (mouse acinar-derived pancreatic cells). On the first day of culture, most cells formed an acinar cell cluster with a high level of amylase. By day 3, a spheroid-like cell aggregate had formed and cells (mAPCs) with a fibroblast-like morphology that were positive for amylase and nestin began to migrate. Proliferation of mAPCs was observed on day 5 and the cells had reached sub-confluence by day 7, but were still positive for nestin. On day 3 of culture the mAPCs were also positive for E-cadherin, an epithelial cell marker, and vimentin, a marker for mesenchymal cells. On day 5, E-cadherin expression remained in cells that adhered with each other, but had disappeared in migrating cells, which still expressed vimentin. These results suggest an epithelial to mesenchymal transition. Further work showed that mAPCs can play an important role of pancreatic carcinogenesis.
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