PR-39 gene transduction suppresses heaptocellular carcinoma cell metastasis by inhibition of signal transduction
| Project/Area Number |
10670444
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | ASAHIKAWA MEDICAL COLLEGE |
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Principal Investigator |
FUJIMOTO Yoshinori Asahikawa Medical College, Medicine Instructor, 医学部, 助手 (90292127)
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| Co-Investigator(Kenkyū-buntansha) |
KOHGO Yutaka Asahikawa Medical College, Medicine Professor, 医学部, 教授 (10133183)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | antimicrobial peptide / PR-39 / syndecan / actin / signal transduction / hepatocellular carcinoma / MAP kinase / 浸潤 |
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| Research Abstract |
PR-39 is an endogenous proline-rich antimicrobial peptide which induces the synthesis of syndecan-1, a transmembrane heparan sulfate proteoglycan involved in cell-to-matrix interactions and wound healing. Previously, we revealed that PR-39 has functions involved in the suppression of motile activity and alteration of actin structure on human hepatocellular carcinoma cells in addition to the suppression of invasive activity which might result from the induction of syndecan-1 expression. To clarify this mechanism we transfected PR-39 gene into NIH3T3 cells transformed with activated k-ras gene. The PR-39 gene transfectant revealed changes of morphology, actin structure, proliferation rate and MAPK activity. PR-39 might affect ras signal transduction.
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Report
(3 results)
Research Products
(7 results)
