| Project/Area Number |
09470243
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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 | 一般 |
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| Research Field |
General surgery
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
OKUSHIBA Shun-ichi Medical Hospital, Hokkaido Univ., Lec., 医学部・附属病院, 講師 (70185536)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIMOTO Masato Fac.of Med., Hokkaido Univ., Lec., 医学部, 講師 (30179585)
KUZUMAKI Noboru Fac.of Med., Hokkaido Univ., Pro., 医学部, 教授 (80091445)
KONDO Satoshi Fac.of Med., Hokkaido Univ., Asso.Pro., 医学部, 助教授 (30215454)
加藤 紘之 北海道大学, 医学部, 教授 (80002369)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥13,400,000 (Direct Cost: ¥13,400,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1997: ¥10,600,000 (Direct Cost: ¥10,600,000)
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| Keywords | Pancreatic Cancer / Cancer Gene Therapy / N116Y / Vector / 遺伝子治療 / アデノウイルスペクター / p53 / K-ras |
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| Research Abstract |
In this study, we tested the efficacy of N116Y in blocking the growth of esophageal cancer cells using an adenoviral vector. Infection with N116Y adenovirus, (AdCMV-N116Y), in which N116Y expression is driven by the cytomegalovirus promoter, significantly reduced the in vitro growth of all esophageal cancer cell lines studied. To examine the suppressive mechanism of N1 16Y, cell cycle profile and the activation of extracellular signal-regulated kinase 2(Erk2) were examined by flow cytometry and Western blot analysis, respectively. In TE8 cells, progression into S phase was clearly blocked after infection with AdCMV-N116Y.Infection with AdCMV-N116Y did not strongly suppress the activation of Erk2 after EGF stimulation in serum-starved HEC46 cells, whereas it completely suppressed activation in TE8, SGF3 and SGF7 cells. Our observations suggest that N116Y reduces growth of human esophageal cancer cells and suppresses the activation of Erk2 ; they also indicate that N116Y is a potential candidate gene for human esophageal cancer gene therapy.
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