2013 Fiscal Year Final Research Report
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
|
Keywords | microRNA / アポトーシス / 炎症性シグナル |
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.
|
-
-
[Journal Article] miR-197 induces epithelial-mesenchymal transition in pancreatic cancer cells by targeting p120 catenin2013
Author(s)
Hamada S, Satoh K, Miura S, Hirota M, Kanno A, Masamune A, Kikuta K, Kume K, Unno J, Egawa S, Motoi F, Unno M, Shimosegawa T
-
Journal Title
J Cell Physiol
Volume: 228(6)
Pages: 1255-1263
DOI
Peer Reviewed
-
-
-
-