2003 Fiscal Year Final Research Report Summary
Development of specific vector containing FN-1 fused protein and SCCA promoter for esophageal cancer
| Project/Area Number |
14370370
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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 |
Digestive surgery
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
OKUSHIBA Shunichi Hokkaido University, Graduate School of Medicine, Asso.Prof., 大学院・医学研究科, 助教授 (70185536)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Masaki Hokkaido University Hospital, University Hospital, Asit, 医学部・歯学部附属病院, 助手 (40333611)
KONDO Satoshi Hokkaido University, Graduate School of Medicine, Asso.Prof, 大学院・医学研究科, 助教授 (30215454)
KATOH Hiroyuki Hokkaido University, Graduate School of Medicine, Prof, 大学院・医学研究科, 教授 (80002369)
TADA Mitsuhiro Hokkaido University, Institute For Genetic Medicine, Asso.Prof, 遺伝子病制御研究所, 助教授 (10241316)
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| Project Period (FY) |
2002 – 2003
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| Keywords | esophageal squamous cell carcinoma / gene therapy / RCAS1 / caveolin-1 / adenoviralvector / SCCA2 promotein |
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| Research Abstract |
We screened several gene expressions in esophageal squamous cell carcinoma (ESCC) for the purpose of finding of cancer specific gene expression and development of therapeutic gene. Then we found that RCAS1 and caveolin-1 are potentially useful for the target of esophageal cancer. Subsequently, we constructed a shuttle vector to make adenoviral vectors in which SCCA2 promoter was introduced. An adenoviral vector which expresses proapoptotic gene KLAKLA2 driven by SCCA2 promoter was reconstructed. Ad-SCCAp-KLAKLAK induced apoptosis in SCCA2 producing cell lines LK2 and LC1, but not A549 or ABC-1 that did not produce SCCA2. Effects of gene therapy using Ad-SCCAp-KLAKLAK were observed in vivo SCCA2 producing tumors implanted on the hack of nude mice were successfully suppressed by Ad-SCCAp-KLAKLAK.
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