Targeting continuous inflammation in pancreatic cancer microenvironment
Project/Area Number |
24790674
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Gastroenterology
|
Research Institution | Tohoku University |
Principal Investigator |
HAMADA Shin 東北大学, 医学(系)研究科(研究院), 助教 (20451560)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | microRNA / アポトーシス / 炎症性シグナル / 浸潤性膵癌 / マイクロRNA / 膵癌組織中炎症 |
Research Abstract |
We assessed the effect of forced expression of miR-365, which was highly expressed in invasive pancreatic cancer compared with IPMN. miR-365 increased the cell viability of pancreatic cancer cells after the gemcitabine treatment, suggesting the induction of resistance. A comprehensive analysis of gene expression profiles in miR-365 introduced cells identified up-regulation of several NF kappa B target genes. Activation of NF kappa B pathway was confirmed by the increased expression of phosphorylated NF kappa B. On the other hand, miR-365 directly targeted apoptosis-related molecules such as SHC1 and BAX that led to the gemcitabine resistance.
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Report
(3 results)
Research Products
(9 results)