| Project/Area Number |
25830092
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
TAKATORI Atsushi 千葉県がんセンター(研究所), がん治療開発グループ, 研究員 (40455390)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | シグナル伝達 / NLRR / 細胞増殖 / 癌 / NLRR1 / 遺伝子改変動物 |
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| Outline of Final Research Achievements |
In the present project, functional analyses of NLRR1 have shown that it promotes tumor growth by regulating various types of receptor tyrosine kinases (RTK) in neuroblastoma (NB). Immunohistochemistry and qPCR have demonstrated that NLRR1 is expressed in various types of adult cancers. Of note, NLRR1 rather suppresses the activation of ALK, a NB-related RTK, through protein-protein interaction. On the other hand, the functional study has indicated a novel role of NLRR2, another member of NLRR family, in drug resistance of NB cells. Overall, the new data from this study suggest that NLRR family proteins contribute to cell fate decision by regulating cell proliferation, survival and differentiation and serve as prognostic factors in NB and other type of cancers.
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