| Project/Area Number |
24591987
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | TAC-101 / 合成レチノイド / Am80 / ATRA / 大腸癌 / 肝転移抑制 / 大腸発癌モデル / 核内レセプター / 分化誘導 |
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| Outline of Final Research Achievements |
4-[3,5-bis(trimethylsilyl)benzamide] benzoic acid (TAC-101) is a novel retinobenzoic acid derivative. All trans retinoic acid (ATRA) and Am80 are already clinical using for treatment of acute promyelocytic leukemia (APL). In this study, for the elucidation of the mechanical action of TAC-101 to inhibit the metastasis of colorectal cancer or carcinogenesis of colorectum, we have researched the changed gene expression of colon cancer cells by TAC-101, ATRA or Am80 using microarray analysis. Gene Ontology analysis and Pathway analysisi were performed to these changed genes selected by microarray analysis. Additionally, immunostaining of these changed genes were performed to the hepatic metastatic tumor and normal liver in rat hepatic metastatic model and colorectal tumor and normal colonic mucosa in rat chemical colon carcinogenesis model. These experiments have indicated the several candidate genes, such as RIP140 (NRIP1), EDAR, GADD153 (DDIT3), targeting by TAC-101.
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