2002 Fiscal Year Final Research Report Summary
Invasion mechanism of Pancreatic cells : the relationship Glial cell line-derived neurotrophic factor and integrin
| Project/Area Number |
13671325
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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 | Nagoya City University |
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Principal Investigator |
TAKEYAMA Hiromitsu Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (00216946)
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| Co-Investigator(Kenkyū-buntansha) |
SAWAI Hirozumi Nagoya City University, Graduate School of Medical Sciences, Rsearch Associate, 大学院・医学研究科, 助手 (40336681)
SATO Mikinori Nagoya City University, Graduate School of Medical Sciences, Research Associate, 大学院・医学研究科, 助手 (20305551)
MANABE Tadao Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (80127141)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Pancreatic / neural invasion / GDNF / RET / GFRalpha-1 / integrin |
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| Research Abstract |
Prineural invasion is a prominent clinical feature of pancreatic cancer. The invasion system forms by multiple steps, but it has not cleared yet. We pay attention to the integrins and investigated its expression and alteration by GDNF. In this study, we use four human pancreatic cancer cell lines which were all found to express the receptor RET and GFRalpha-1 for GDNF. In the invasion assay, all human pancreatic cancer cell lines stimulated by GDNF increased the invasive ability for ECMs. In the adhesion assay, they increased the adhesive ability for ECMs. All pancreatic cancer cell lines stimulated by GDNF, their adhesive and the invasive ability in inhibited by anti-RET antibody, anti-GFRalpha-1 antibody and anti-betal antibody. In the flow-cytometric analysis, the integrin subunit alpha2, alpha3, alpha5, alpha6 and betal expressed in the all pancreatic carcinoma cell lines. In the cellular enzyme-linked immunosorbent assay, the integrin subunit expressed strongly under stimulating by GDNF. In the all pancreatic cancer cell lines, the expression of integrin subunit, the invasive ability and the adhesive ability appeare to increase under stimulating by GDNF. NF-kappaB was enhanced in the all pancreatic tumor cells stimulated by GDNF. We conclude that GDNF and integrin have very important role for the neural' invasive system of pancreatic cancer cells. We suggest that the control of the receptor or integrin makes new therapy.
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