| Project/Area Number |
15K21288
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
General pharmacology
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| Research Institution | Osaka City University |
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Principal Investigator |
Otani Koji 大阪市立大学, 大学院医学研究科, 講師 (30597555)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 炎症発癌 / プロスタグランジントランスポーター / プロスタグランジン / 大腸癌 / 潰瘍性大腸炎 |
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| Outline of Final Research Achievements |
Prostaglandin (PG) E2 promotes gastrointestinal carcinogenesis. The total amount of active PGE2 is regulated by the PG biosynthesis and degradation pathways which include cyclooxygenase-2 (COX-2: PG synthase), 15-hydroxyprostaglandin dehydrogenase (15-PGDH: catabolic enzyme of PG), PG transporter (PGT: influx transporter), and multidrug resistance associated protein 4 (MRP4: efflux transporter). We examined the expression of PGT, which transports PG into cell for its metabolic degradation, and the other molecules in colitis-associated carcinogenesis. Increased expression of COX-2 and MRP4 and decreased expression of 15-PGDH and PGT were observed in colon cancer part, and PGE2 contest in colon cancer cell was elevated. PGT expression and PGE2 content were regulated by TNF-α, and it was suggested that there was a function linkage between PGT and 15-PGDH.
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