2005 Fiscal Year Final Research Report Summary
Study of the mechanisms of cancer prevention by food factors for personalized prevention
| Project/Area Number |
16590479
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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 |
Hygiene
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
SOWA Yoshihiro Kyoto Prefectural University of Medicine, Graduate School of Medical Sciences, Assistant Professor, 医学研究科, 講師 (70315935)
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| Project Period (FY) |
2004 – 2005
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| Keywords | cancer prevention / food factor / genistein / apigenin / fucoxantin / artepillin C / sulforaphane / molecular-targeting cancer prevention |
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| Research Abstract |
As for the relation between cancer and the meal, implications are suggested as a cancer prevention factor there are a lot of uncertain points of the action mechanism of the cancer prevention though it is reported that a variety of cancer prevention factors are actually included in food. Then, the research that clarified the action mechanism was executed to the food factor from which the cancer prevention effect was reported.
We studied the action mechanisms of genistein, that is flavonoid included in the soybeans, apigenin, that is also flavonoid included in green vegetables, fucoxantin, that is natural carotenoid included in seaweeds, artepillin C, that is an element of bee products, propolis, and sulforaphane, that is isothiocyanate such as isothiocyanate sulforaphane included in crucifer vegetables.
Genistein inhibited the proliferation of the cancer cell by inducing the gadd45 gene. Apigenin inhibited the proliferation of the cancer cell by inducing the p21/WAF1 gene. Both fucoxantin and artepillin C also induced the p21/WAF1 gene and inhibited the proliferation of the cancer cell.
These results suggest the possibility of the development of the molecular target cancer preventive that makes gadd45 and p21/WAF1 target molecules. We found that the sulforaphane induced DR5 that is the receptor molecule of TRAIL that was the apoptosis inducible cytokine. As the result, apoptosis is enabled to be induced to the cancer cell by the low concentration of TRAIL treatment in inducing DR5 by sulforaphane, and these results suggest the development of the molecular-targeting combination cancer preventive using together of sulforaphane and TRAIL that makes DR5 target molecule.
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