Identification and functional analysis of nuclear pore complex components that function to transport beta-catenin between cytoplasm and nucleus
| Project/Area Number |
15K15493
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
WONG Richard 金沢大学, 自然システム系, 教授 (30464035)
ISHIGAKI Yasuhito 金沢医科大学, 総合医学研究所, 教授 (20232275)
OHTA Tetsuo 金沢大学, 医学系, 教授 (40194170)
MIYASHITA Tomoharu 金沢大学, 附属病院, 助教 (30397210)
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| Research Collaborator |
DOMOTO Takahiro 金沢大学, がん進展制御研究所, 助教 (80635540)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 大腸がん / β-カテニン / 核移送 / 核膜孔複合体 |
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| Outline of Final Research Achievements |
To understand the mechanism by which β-catenin with no nuclear localization signal transits between cytoplasm and nucleus, this study investigated expression of and interaction between β-catenin and nucleoporins (Nups) that constitute nuclear pore complex and participate in nucleocytoplasmic trafficking of various functional macro-molecules. Comparative analysis of expression of 30 Nups in normal cells, colon cancer cell lines, human colorectal cancer (CRC) tissues and the non-neoplastic mucosa found an inverse association between the expression of a certain Nup (here called NupX) and the nuclear accumulation of β-catenin in colon cancer cells and CRC tissues. Subsequent analysis identified NupX among Nups coimmunoprecipitated with β-catenin and T-cell factor (Tcf)4 in protein extracts from colon cancer SW480 and HCT116 cells. Analysis of its expression and function indicated that NupX functions to excrete β-catenin from nucleus, thereby inactivating the Wnt signal pathway in CRC.
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Report
(3 results)
Research Products
(31 results)
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[Journal Article] Glycogen synthase kinase 3β sustains invasion of glioblastoma via the focal adhesion kinase, Rac1 and c-Jun N-terminal kinase-mediated pathway.2015
Author(s)
Chikano Y, Domoto T, Furuta T, Sabit H, Kitano-Tamura A, Ilya V. Pyko, Takino T, Sai Y, Hayashi Y, Sato H, Miyamoto K, Nakada M, MinamotoT.
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Journal Title
Molecular Cancer Therapeutics
Volume: 14
Issue: 2
Pages: 564-574
DOI
Related Report
Peer Reviewed / Open Access
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