Establishment of the novel treatment strategy against urothelial carcinoma controlling for the transcription factors
| Project/Area Number |
23592349
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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 |
Urology
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| Research Institution | Keio University |
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Principal Investigator |
KIKUCHI Eiji 慶應義塾大学, 医学部, 講師 (10286552)
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| Co-Investigator(Kenkyū-buntansha) |
OYA Mototsugu 慶應義塾大学, 医学部, 教授 (00213885)
MIYAJIMA Akira 慶應義塾大学, 医学部, 講師 (90245572)
TANAKA Nobuyuki 慶應義塾大学, 医学部, 講師(非常勤) (60445244)
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
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)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 尿路上皮癌 / 抗癌剤 / シグナル伝達 / 喫煙 |
|---|
| Research Abstract |
The following five results were obtained.(1)We identified that the close association between E-, P-cadherin expression and clinico-pathological features and that Snail expression is an independent prognostic factor.(2)In CDDP-resistant cell line; T24PR, we confirmed that PI3K-Akt-mTOR signal was elevated and NVP-BEZ235 could inhibit the PI3K-Akt-mTOR signal and induce the cytotoxic effect. (3)By nicotine exposure, the pAkt was activated and cell viability and tumor growth increased in T24 cells. (4)In the T24PR cell, DHMEQ which is a novel NF-kappaB inhibitor could inhibit the activation of NF-kappaB, the cell viability, and tumor growth.(5)In the T24PR cell, significant anticancer efficacy was observed in the combination of DHMEQ with Paclitaxel.
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Report
(4 results)
Research Products
(10 results)
