| Project/Area Number |
13671363
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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 |
Digestive surgery
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
TANAKA Toshiaki Kurume University School of Medicine, Department of Surgery, Instructor, 医学部, 助手 (20227151)
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| Co-Investigator(Kenkyū-buntansha) |
SHINOZAKI Kouji Kurume University School of Medicine, Department of Surgery, Instructor, 医学部, 助手 (70226140)
YAMANA Hideaki Kurume University School of Medicine, Department of Surgery, Professor, 医学部, 教授 (30140669)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | esophageal cancer / PPARγ / cell cycle / cell differentiation |
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| Research Abstract |
We investigated the expression of peroxisome proliferator-activated receptor (PPAR) γ in human esophageal squamous cell carcinomas and the effect of PPARγ ligand on cell growth in esophageal cancer. Reverse transcription-polymerase chain reaction and Western blot analysis showed that human esophageal cancer cell lines, KE-5, KE-8 and KE-10, expressed PPARγ mRNA and protein. Cell growth of these cells were inhibited after treatment with PPARγ ligand, troglitazone, in a dose-dependent manner. Flow cytometric analysis demonstrated G1 cell cycle arrest and positive rate of Ki-67 staining was significantly decreased after troglitazone treatment. These results suggested that antiproliferative effect of PPARγ ligand in esophageal cancer is in part induced by negative effect on the cell cycle. Involucrin is expressed in squamous epithelial cells and has been used as a standard marker of terminal differentiation of squamous cells. Troglitazone treatment induced increased expression of involucrin in esophageal cancer cells, indicating that PPARγ ligand augmented cell differentiation in esophageal cancer cells. Furthermore, we examined whether PPARγ ligand induced apoptosis in these cells or not. There was no DNA fragmentation observed after troglitazone treatment, meaning that apoptosis was not involved in antiproliferative effect of PPARγ ligand in esophageal cancer. Finally, we examined the effect of troglitazone on tumor growth in vivo. We observed no difference in tumor growth between treated and untreated group.
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