The novel mechanisms of sonic hedgehog gene expression in the chronic inflammation induced cancer
Project/Area Number |
25870792
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
General medical chemistry
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Research Institution | Nippon Medical School |
Principal Investigator |
Abe Yoshinori 日本医科大学, 付置研究所, 助教 (00386153)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | STAT3 / hedgehogシグナル伝達経路 / 肺癌 / hedgehog経路 / 癌化の分子機構 / Hedgehogシグナル伝達経路 / 非小細胞肺癌 / 慢性炎症 / 遺伝子転写制御 |
Outline of Final Research Achievements |
Lung cancer is the most leading cause of cancer death. We found that the expression of sonic hedgehog (Shh) gene, which is a ligand required for hedgehog signaling pathway activation was enhanced in lung cancer-derived cell lines. From subsequent analysis, we found that a transcription factor STAT3, which is involved in the chronic inflammation-induced tumorigenesis, induced Shh gene expression in lung cancer-derived cell lines. This mechanism may play an important role in tumor maintenance.
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Report
(4 results)
Research Products
(4 results)