2015 Fiscal Year Final Research Report
Development of a new molecular target for glioma mediated ribosome synthesis inhibition (nucleolar stress)
Project/Area Number |
26861164
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Neurosurgery
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Research Institution | Keio University |
Principal Investigator |
MIWA TOMORU 慶應義塾大学, 医学部, 助教 (20365282)
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Project Period (FY) |
2014-04-01 – 2016-03-31
|
Keywords | EFTUD1 / glioma / ribosome |
Outline of Final Research Achievements |
EFTUD1 expression in glioma cell lines and tissue was higher than in normal brain tissue. Downregulating EFTUD1 induced G1 cell-cycle arrest and apoptosis, leading to reduced glioma cell proliferation. The mechanism underlying this antitumor effect was impaired ribosome biogenesis via EFTUD1 inhibition. Additionally, protective autophagy was induced by glioma cells as an adaptive response to EFTUD1 inhibition. The antitumor effect induced by the combined treatment was significantly higher than that of either EFTUD1 inhibition or CQ alone. These results suggest that EFTUD1 represents a novel therapeutic target and that the combination of EFTUD1 inhibition with autophagy blockade may be effective in the treatment of gliomas.
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Free Research Field |
脳神経外科
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