| Project/Area Number |
25861450
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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 |
Urology
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| Research Institution | Keio University |
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Principal Investigator |
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| Research Collaborator |
KIKUCHI Eiji 慶應義塾大学, 医学部, 講師 (10286552)
MIYAJIMA Akira 慶應義塾大学, 医学部, 准教授 (90245572)
OYA Mototsugu 慶應義塾大学, 医学部, 教授 (00213885)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 膀胱癌 / NVP-BEZ235 / mTOR / 膀胱内注入 / 膀胱内注入療法 |
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| Outline of Final Research Achievements |
NVP-BEZ235 inhibited the viability of MBT-2 cells in a dose-dependent manner. Furthermore, the expression of pAkt, pS6, and p4EBP1 was inhibited in NVP-BEZ235-treated MBT-2 cells. Orthotopic models were established by implanting MBT-2 cells into the bladders of female C3H/He mice. Bladder weights were significantly lower in the NVP-BEZ235-treated group than in the control group (P < 0.05). An analysis of the tumor tissues revealed that the NVP-BEZ235 treatment strongly reduced pAkt, pS6, and p4EBP1 levels. An immunohistochemical analysis showed that NVP-BEZ235 significantly inhibited the expression of pS6. Intravesically administered NVP-BEZ235 exerted significant antitumor effects in the orthotopic bladder cancer model by inhibiting the PI3K/AKT/mTOR pathway. The intravesical instillation of a dual PI3K/mTORC1/2 inhibitor may represent a novel therapy for the treatment of bladder cancer.
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