| Project/Area Number |
25861204
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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 |
Digestive surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
HIRASHIMA Kotaro 熊本大学, 医学部附属病院, 非常勤診療医師 (10594468)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | mTOR / 食道扁平上皮癌 / mTOR阻害剤 / 抗癌剤感受性 / Hedgehogシグナル / RAD001 / PI3K/AKT / Gli1 / hedgehog / cell cycle |
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| Outline of Final Research Achievements |
The mammalian target of rapamycin (mTOR) plays a crucial role in protein translation, cell growth, and proliferation. The aberrant activation of mTOR and its prognostic significance have been reported in several cancers, including esophageal squamous cell carcinoma (ESCC). We investigated that the mTOR pathway was aberrantly activated in most ESCC tumors, mTOR inhibitor had a therapeutic effect on mTOR-activated ESCC cell both in vitro and in vivo. After having measured p-mTOR level of ESCC, we classified expression level. We examined both cell in invasion ability, growth ability, antiapoptosis, antitumor effect by mTOR inhibitor. We confirmed that expression of p-mTOR were important. Moreover, we made mice with ESCC and confirmed an antitumor effect with mTOR inhibitor. We identified that the p-mTOR positive case significantly was poor prognosis. In the Hedgehog signaling, we did not recognize the significance for the expression of Gli1.
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