| Project/Area Number |
07557339
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 試験 |
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| Research Field |
Gastroenterology
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| Research Institution | KYOTO PREFECTURAL UNIVERSITY OF MEDICINE |
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Principal Investigator |
MATSUKAWA Yoshizumi KYOTO PREFECTURAL UNIVERSITY,MEDICAL DEPARTMENT,AN ASSISTANT, 医学部, 助手 (00254368)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUNO Takakazu CHUGAI RESEARCH INSTITUTE MORECULAR MEDICINE,A LEADER OF THE SECOND TRAM (A SCIE, 第2チームリーダー
NOMURA Hitoshi CHUGAI RESEARCH INSTITUTE FOR MOLECULAR MEDICINE,AN ACTING HEAD (A SCIENTIST), 所長代行
SAKAI Toshiyuki KYOTO PREFECTURAL UNIVERSITY,MEDICAL DEPARTMENT,PROFESSOR, 医学部, 教授 (20186993)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1996: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | COLON CANCER / BUTYRATE / G1 ARREST / WAF1 / Cip1 / PROMOTER |
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| Research Abstract |
Butyrate is well known colonic luminal short chain fatty acid, which arrests cell growth and induces differentiation in varied cell types. We examined the effect of butyrate on the expression of WAF1/Cip1, a potent inhibitor of cycline-dependent kinases, and its relation to growth arrest in a p53-mutated human colon cancer cell line WiDr. Five millimolar butyrate completely inhibited the growth of WiDr and caused G1-phase arrest. WAF1/Cip1 mRNA was rapidly induced within 3 hours by treatment with 5.0 mM butyrate, and drastic WAF1/Cip1 protein induction was detected. Using several mutant WAF1/CIP1 promoter fragments, butyrate increased the promoter activity in the reporter plasmid with or without p53 binding sites. These findings suggest that butyrate arrests the growth of WiDr cells by activating the WAF1/Cip1 promoter in a p53-independent fashion.
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