2001 Fiscal Year Final Research Report Summary
Signal transduction system responsible for the retraction of vascular endothelial cells upon cancer cell invasion or metastasis
| Project/Area Number |
12671224
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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 | Osaka University |
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Principal Investigator |
ARIYOSHI Hideo Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (60294055)
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| Co-Investigator(Kenkyū-buntansha) |
SAKON Masato Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (40170659)
NAKAMORI Shoji Osaka University, Graduate School of Medicine, Lecturer, 医学系研究科, 講師 (70294080)
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| Project Period (FY) |
2000 – 2001
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| Keywords | cancer invasion / cancer metastasis / EC retraction / cytoplasmic ionized Ca2+ |
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| Research Abstract |
It is well known that the loss of VEC integrity plays pivotal roles in several physiological or pathological phenomena, such as inflammation or cancer metastasis. In this study, we studied the possible involvement of cytoplasmic ionized Ca2+ ([Ca2+]i) in VEC retraction induced by cancer cells. The mode of vEC activation by direct cell-to-cell contact or cancer cell secreted soluble factors was separately analyzed. Digital imaging analysis using Ca2+ indicator, fluo-3, cleary demonstrated [Ca2+]i oscillation in human umbilical vein endothelial cells (HUVECs) upon cell contact with human breast cancer cell line, MCF-7, which was not inhibited by extracellular Ni2+ and was inhibited by pretreating the cells by paraformaldehyde. Although culture medium derived from MCF-7 also caused VEC retraction aァ well as [Ca2+]i oscillation, the former was inhibited by the heat-treatment of the culture medium, suggesting that [Ca2+]i osillation is not essential in VEC retraction induced by cancer derived soluble factors.
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Research Products
(8 results)
