2016 Fiscal Year Final Research Report
Analysis of the pathway of Smo transcription for development of new therapeutic strategy inhibiting Hedgehog signaling
Project/Area Number |
26293289
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
General surgery
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Research Institution | Kyushu University |
Principal Investigator |
ONISHI HIDEYA 九州大学, 医学研究院, 准教授 (30553276)
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Co-Investigator(Kenkyū-buntansha) |
中野 賢二 九州大学, 先端融合医療レドックスナビ研究拠点, 教授 (00315061)
野村 政壽 九州大学, 大学病院, 講師 (30315080)
久保 真 九州大学, 大学病院, 助教 (60403961)
中村 勝也 九州大学, 医学(系)研究科(研究院), 共同研究員 (60585743)
山崎 章生 九州大学, 医学(系)研究科(研究院), 共同研究員 (80404440)
片野 光男 九州大学, 医学(系)研究科(研究院), 教授 (10145203)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 膵癌 / Hedgehogシグナル / Smoothened / 低酸素環境 / 悪性形質誘導 / 増殖能 / 浸潤能 / 転写活性 |
Outline of Final Research Achievements |
We found that transcriptional factor, recombination signal binding protein for immunoglobulin-kappa-J region (RBPJ) and transcriptional coactivator, mastermind like-3 (MAML3) contribute to the mechanism of upregulation of Smootnened (SMO) transcription under hypoxia, and that inhibition of RBPJ/MAML3 signaling suppress the inducing of malignant phenotype such as proliferation, invasion and tumorigenesis in pancreatic cancer.
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Free Research Field |
臨床腫瘍学
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