2015 Fiscal Year Final Research Report
Sensitivity of chemotherapy in pancreatic cancer cells
| Project/Area Number |
25462128
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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 |
Digestive surgery
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KUNIYASU Hiroki 奈良県立医科大学, 医学部, 教授 (00253055)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | Gemcitabine耐性膵癌 |
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| Outline of Final Research Achievements |
We established GEM-resistant cells (MIA-GEMR) from MIA PaCa-2 cells and analyzed signaling pathway associated with the KRAS mutation MIA-GEMR cells showed the epithelial-mesenchymal transition phenotype and invasiveness, which were similarly induced by the KRAS mutation in colorectal cancer cells. The genes differentially expressed between MIA-GEMR and MIA PaCa-2 cells were compared with those observed between the human colorectal cancer HCT116 cells and HKe3 cells. Notably, the common genes associated with mutant KRAS regulation overlapped with stem cell-specific genes and TGF-β1 target genes, suggesting the crucial role of mutant KRAS in determining the morphology and microenvironment. Furthermore, the phosphodiesterase inhibitor resveratrol suppressed the growth of MIA-GEMR. These results suggest that TGF-β1 signaling downstream of oncogenic KRAS is involved in the onset of GEM resistance in MIA PaCa-2 cells.
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| Free Research Field |
胆膵外科
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