2005 Fiscal Year Final Research Report Summary
Inhibition of cell growth and cell invasion by PPAR gamma in GI cancers
| Project/Area Number |
16590568
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
OKUMURA Toshikatsu Asahikawa Medical College, Department of General Medicine, Professor, 医学部, 教授 (60281903)
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| Co-Investigator(Kenkyū-buntansha) |
TANNO Satoshi Asahikawa Medical College, Department of General Medicine, Assistant Professor, 医学部, 講師 (30333686)
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| Project Period (FY) |
2004 – 2005
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| Keywords | troglitazone / extracellular signal releted kinase / mitogen-activated protein kinase kinase / pancreatic cancer cells / growth inhibition / PPARγ / 細胞増殖抑制 / アポトーシス |
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| Research Abstract |
In the present study, we examined a role of mitogen-activated protein kinases (MAPKs), extracellular signal releted kinase (ERK), c-Jun N-terminal protein kinase (JNK) and p38 MAPK in troglitazone-induced inhibition of cell growth in human pancreatic cancer cells. Among the three kinases, troglitazone specifically inhibited the phosphorylation of ERK1/2 in a dose- and time-dependent manner. Troglitazone also down-regulated the protein expression of mitogen-activated protein kinase kinase (MEK)1/2, an upstream molecule that regulates ERK phosphorylation. Treatment of human pancreatic cancer cells with specific MEK inhibitor, PD98059 or U0126 inhibited ERK1/2 phosphorylation and cell growth. These results suggest for the first time that the inhibition of the MEK1/2-ERK1/2 signaling pathway may be implicated in the growth inhibitory effect by troglitazone in human pancreatic cancer cells.
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