Project/Area Number |
04670410
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Gastroenterology
|
Research Institution | University of Tokyo |
Principal Investigator |
KANEKO Yoshiyasu Faculty of Medicine, Lecturer, 医学部(病), 講師 (90124669)
|
Co-Investigator(Kenkyū-buntansha) |
KOIKE Kazuhiko Faculty of Medicine, Assistant, 医学部(病), 助手 (80240703)
NAKAYAMA Toshibumi Faculty of Medicine, Assistant, 医学部(病), 医員 (80150275)
HASHIMOTO Yoshiaki Faculty of Medicine, Assistant, 医学部(病), 助手 (40172879)
|
Project Period (FY) |
1992 – 1993
|
Project Status |
Completed (Fiscal Year 1993)
|
Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
Keywords | hepatoma / hepatitis virus / tumor promoter / apoptosis / calcium / anti-oncogene / 肝炎ウィルス / 肝癌 / 癌遺伝子 / B型肝炎ウイルス / C型肝炎ウイルス / 転写調節 |
Research Abstract |
Tumor promoter teleocidin stimulates protein kinase C of pLC/pRF/5 hepatoma cells which is structurally different from that of other kinds of cells. Teleocidin inhibits apoptosis of the hepatoma cells induced by mitomycin C and etoposide. Thapsigargin depletes endoplasmic reticulum calcium pool, and induces apoptosis of the hepatoma cells. Thapsigargin-induced apoptosis is not associated with an increased nuclear p53, while apoptosis induced by mitomycin C and etoposide is preceded by nuclear p53 accumulation. Therefore, tumor promoters may enhance carcinogenesis by modulating apoptotic processes. A possibility that hepatities viruses enhance hepatoma development by similar mechanism has been studied.
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