| Project/Area Number |
23592546
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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 |
Otorhinolaryngology
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| Research Institution | Ohu University (2013)
独立行政法人国立病院機構(東京医療センター臨床研究センター) (2011-2012) |
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Principal Investigator |
BABA YUH 奥羽大学, 歯学部, 准教授 (40597663)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Masato 国立病院機構東京医療センター, 聴覚平衡覚研究部, 部長 (70129633)
|
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| Co-Investigator(Renkei-kenkyūsha) |
KATO Yasumasa 奥羽大学, 歯学部, 教授 (50214408)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 頭頸部癌 / デグエリン / EGFR / IGF1R / AKT / ERK / EGFR阻害剤耐性 / EGFR阻害剤 / 耐性 / 頭頸部扁平上皮癌 / EGFRインヒビター耐性 / クロストーク |
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| Research Abstract |
Despite advances in the management of head and neck squamous cell carcinoma (HNSCC) patients, the survival has not been significantly improved. Therefore, the search for potential alterative therapies is encouraging. In the current study, we examined the effect of deguelin, a rotenoid from the African plant Mundulea sericea on head and neck squamous cell carcinoma cell lines. The results demonstrated that deguelin induced apoptosis by inhibiting constitutive and EGF-stimulated AKT activation. We further demonstrated that deguelin inhibited IGF1R-AKT pathway.
Cetuximab, antibody of EGFR, is an applicable for HNSCC therapy. However, a mechanism of cetuximab resistance for HNSCC is thought to be IGF1R-AKT signaling in addition to EGFR-AKT pathway. Therefore, these results suggested that deguelin may overcome resistance to EGFR inhibitor in HNSCC. Further work is needed.
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