2006 Fiscal Year Final Research Report Summary
Hypoxia-to-reoxygenation condition as one of the internal carcinogenic factors of common cancers
| Project/Area Number |
17590334
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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 |
Experimental pathology
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| Research Institution | Yamagata University |
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Principal Investigator |
OKADA Futoshi Yamagata University, Department of Biomolecular Function, Graduate School of Medical Science, Associate Professor, 大学院医学系研究科, 助教授 (00250423)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Junichi Yamagata University, Department of Biomolecular Function, Graduate School of Medical Science, Professor, 大学院医学系研究科, 教授 (00222258)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Hypoxia reperfusion / Free radical / Carcinogenesis / DNA microarray / Proteomics |
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| Research Abstract |
We examined whether free radicals generated in a series of ischemia-reperfusion condition could act as an endogenous carcinogenic factor in normal or premalignant cells. We obtained various cell lines from human epithelial cells, rodent immortalized fibroblasts and benign fibrosarcoma cells to examine whether those cell lines could be converted into tumorigenic ones after cultivation in a series of hypoxia-reoxygenation condition. Free radicals were produced in the cells after they were cultured in the hypoxia-reoxygenation condition. Peroxides, a part of free radicals, were detected by using the specific probe 2', 7'-dichlorodihydrofluorescein diacetate (H2DCFDA). The production of peroxides was suppressed by an addition of several free radical scavengers into the culture medium. Among those cell lines, non-tumorigenic mouse fibroblast cell lines were converted into tumorigenic ones in nude mice. We then compared their gene/protein expressions with their normal counterparts. We have identified two genes possibly related with carcinogenesis by combinational analyses of DNA microarray and two-dimensional protein electrophoresis. The expression of the two genes decreased in the tumorigenic cells compared to parent cells. We found that one of the two genes actually regulated tumorigenic potential of the mouse fibroblast cells. We expect to further confirm this finding after examining expressions of those genes in a variety of human tumor tissues and rodent spontaneous arising tumors.
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Research Products
(17 results)
