| Project/Area Number |
22700920
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Clinical oncology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TAKAHASHI Tetsuyuki 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (00403692)
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|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
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| Keywords | エイコサノイド / エイコサノイド受容体 / 癌 |
|---|
| Research Abstract |
The soluble prostaglandin E_2 receptor(FuEP2/ Ex2) suppressed cancer cell growth and production of hemorrhagic ascites in an orthotopic xenograft model of endometrial cancer and intraperitoneal dissemination model of ovarian cancer. In endometrial cancer, we also revealed that this inhibition was associated with suppression of ERK1/ 2-phosphorylation and COX-2, VEGF, and c-fos mRNA induction, which are consequences of EP receptor-elicited cellular signaling. By using conditional expression system which can be controlled by doxycycline, we obtained stable transfectant of 15-hydroxyprostaglandin dehydrogenase(15-PGDH) derived from human pancreas cancer cell line. We found that expression of 15-PGDH causes decrease of cell growth and survival rate, desensitization to insulin-and epidermal growth factor-induced cell growth, and sensitization to TNF-related apoptosis inducing ligand-induced apoptosis.
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