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Physiological significance of EGF/STAT1 pathway

Research Project

Project/Area Number 11680671
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Molecular biology
Research InstitutionChiba University

Principal Investigator

KITAGAWA Motoo  Chiba University, School of Medicine Associate Professor, 医学部, 助教授 (40262026)

Co-Investigator(Kenkyū-buntansha) HARIGAYA Kenichi  Chiba University, School of Medicine Professor, 医学部, 教授 (40101894)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
KeywordsSTAT / EGF / Signal transduction / Esophageal Cancer / Tumor progression / Tumor suppressor / tumor suppressor
Research Abstract

In only a very limited number of cultured cell lines, epidermal growth factor (EGF), a potent mitogen for many kinds of cells, was shown to activate STAT1 (for signal transducer and activator of transcription 1) protein, which can transmit signals causing cell growth arrest and apoptosis. To elusidate physiological and/or pathological significance of this EGF-STAT1 pathway, a series of cultured cell lines which had been established from surgical specimens of esophageal squamous cell carcinoma was studied for the existence of the EGF-STAT1 pathway. EGF treatment leads to a strong growth arrest in three among the 30 esophageal squamous cell carcinoma cell lines. STAT1 was found to be activated by EGF in the three cell lines but not in the others. EGF can also activate STAT1 in cultured normal esophageal squamous epithelial cells. STAT1 is at the activated state in the basal cell layer of the bovine esophageal epithelium. Notably patients who had harbored the cancer cells with the EGF-STAT1 pathway underwent dramatically better prognosis. Thus, the EGF-STAT1 pathway may be intrinsic to esophageal epithelial lineage of cells, and is lost in a considerable fraction of the carcinomas. This loss appears to cause significantly more malignant clinical course to the patients. These findings may point out a critical step in the progression of the esophageal cancer and could lead to the development of useful clinical applications.

Report

(2 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • Research Products

    (18 results)

All Other

All Publications (18 results)

  • [Publications] Li C.et al: "A Lys644Glu substitution in fibroblast growth factor receptor 3(FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors."Hum.Mol.Gen.. 8. 35-44 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Matsumoto M.et al: "Activation of the transcription factor ISGF3 by interferon-γ."Biol.Chem.. 380. 699-703 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Qiang, Y.-W.et al.: "Activation of mitogen-activated protein kinase through α5/β1 integrin is required for cell cycle progression of B progenitor cell line, Reh, on human marrow stromal cells."Exp.Hematol.. 28. 1147-1157 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Watanabe G.et al.: "progression of esophageal carcinoma by loss of EGF-STAT1 pathway."Cancer J.. (in press). (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Xie B.et al.: "Focal adhesion kinase activates Stat1 in integrin-mediated cell migration and adhesion."J.Biol.Chem.. (in press). (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Kitagawa M.et al.: "A human protein with sequence similarity to Drosophila Mastermind coordinates the nuclear form of Notch and a CSL protein to build a transcriptional activator complex on target promoters."Mol.Cell.Biol.. (in press). (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Li C., Chen L., Iwata T., Kitagawa M., Fu X.-Y.and Deng C.-X.: "A Lys644Glu substitution in fibroblast growth factor receptor 3 (FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors."Hum.Mol.Gen.. 8. 35-44 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Matsumoto M., Tanaka N., Harada H., Kimura T., Yokochi T., Kitagawa M., Schindler C.and Taniguchi T.: "Activation of the transcription factor ISGF3 by interferon-γ."Biol.Chem.. 380. 699-703 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Qiang, Y.-W., Kitagawa.M., Higashi, M., Ishii, G., Morimoto, C., and Harigaya, K.: "Activation of mitogen-activated protein kinase through α5/β1 integrin is required for cell cycle progression of B progenitor cell line, Reh, on human marrow stromal cells."Exp.Hematol.. 28. 1147-1157 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Watanabe G., Kaganoi J., Imamura M., Shimada Y., Itami A., Uchida S., Sato F., and Kitagawa M.: "Progression of esophageal carcinoma by loss of EGF-STAT1 pathway."Cancer J.. 7(in press). (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Xie B., Zhao J., Kitagawa M., Durbin J., Madri J.A., Guan J.-L., and Fu X.-Y.: "Focal adhesion kinase activates Stat1 in integrinmediated cell migration and adhesion."J.Biol.Chem.. (in press). (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Kitagawa M., Oyama T., Kawashima T., Yedvobnick B., Kumar A., Matsuno K., and Harigaya K.: "A human protein with sequence similarity to Drosophila Mastermind coordinates the nuclear form of Notch and a CSL protein to build a transcriptional activator complex on target promoters."Mol.Cell.Biol.. (in press). (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Li C. et al.: "A Lys644Glu substitution in fibroblast growth factor receptor 3 (FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors."Hum.Mol.Gen.. 8. 35-44 (1999)

    • Related Report
      2000 Annual Research Report
  • [Publications] Matsumoto M. et al: "Activation of the transcription factor ISGF3 by interferon-γ."Biol.Chem.. 380. 699-703 (1999)

    • Related Report
      2000 Annual Research Report
  • [Publications] Qiang,Y.-W. et al.: "Activation of mitogen-activated protein kinase through α5/β1 integrin is required for cell cycle progression of B progenitor cell line, Reh, on human marrow stromal cells."Exp.Hematol.. 28. 1147-1157 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Watanabe G. et al.: "Progression of esophageal carcinoma by loss of EGF-STAT1 pathway."Cancer J.. (in press). (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] Xie B. et al.: "Focal adhesion kinase activates Stat1 in integrin-mediated cell migration and adhesion."J.Biol.Chem.. (in press). (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] Kitagawa M. et al.: "A human protein with sequence similarity to Drosophila Mastermind coordinates the nuclear form of Notch and a CSL protein to build a transcriptional activator complex on target promoters."Mol.Cell.Biol.. (in press). (2001)

    • Related Report
      2000 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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