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Role of cytokine-inducible transcription factors in renal cell carcinoma

Research Project

Project/Area Number 15591715
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Urology
Research InstitutionKeio University

Principal Investigator

OYA Mototsugu  Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (00213885)

Co-Investigator(Kenkyū-buntansha) MARUMO Ken  Keio University, School of Medicine, Associate Professor, 医学部, 助教授 (80138130)
MURAI Masaru  Keio University, School of Medicine, Professor, 医学部, 教授 (90101956)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
KeywordsRenal cell carcinoma / cytokine / apoptosis / NF-κB / C / EBP / AP-2 / MAP kinase / Akt / EBP-β
Research Abstract

Renal cell carcinoma(RCC) is occasionally associated with paraneoplastic syndromes such as inflammatory reactions and leukocytosis. Cytokines produced by cancer cells are considered to accelerate cell growth in an autocrine or paracrine manner as well as induce cahexic reactions to the host. Furtheremore, Cytokine-dependent signal transduction has been implicated to play a role in maintaining cancer cell survival. Therefore, blocking the signal pathways may have a therapeutic potential for RCC. Transcription factors not only induce de novo cytokine expression, but their activities are also induced by cytokines and therefore may play a substantial role in cytokine-mediated autocrine growth in RCC. Increased activation of NF-κB, STAT3 and C/EBP-β were associated with a high tumor stage and grade. PI3K-Akt pathway has been implicated to regulate key effector molecules involved in controlling the balance of cell survival and apoptosis. Akt activation determined by immunohistochemistry associated with high tumor grade and metastatic disease. Immunoblotting studies revealed decreased PTEN expression is necessary but not sufficient for Akt activation. Akt inhibitor induced apoptosis in some RCC cell lines. MAP kinases include ERKs, JNK, and p38. ERKs are constitutively activated, but JNK and p38 are inactivated in a steady state of RCC. ERKs inactivation did not induce apoptosis, therfore, ERKs do not seem to relate to cell survival. In contrast, inductive JNK or p38 activation induced apoptosis in some RCC cell lines. Our investigation of signal transduction pathways shed some light on a potential novel treatment for RCC. These signal trasduction molecules mentioned above are candidates for molecular targeting therapy for RCC.

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • Research Products

    (13 results)

All 2004 2003 Other

All Journal Article (11 results) Publications (2 results)

  • [Journal Article] Differential expression of activator protein-2 isoforms in renal cell carcinoma.2004

    • Author(s)
      Oya, M., Mikami, S., Mizuno, R., Miyajima, A., Horiguchi, Y., Nakashima, J., Marumo, K., Mukai, M., Murai, M.
    • Journal Title

      Urology 64

      Pages: 162-167

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Inhibition of MKP-1 expression potentiates JNK related apoptosis in renal cancer cells.2004

    • Author(s)
      Mizuno, R., Oya, M., Shiomi, T., Marumo, K., Okada, Y., Murai, M.
    • Journal Title

      Journal of Urology 172

      Pages: 723-727

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Inhibition of the ubiquitin-proteasome pathway activates stress kinases and induces apoptosis in renal cancer cells.2004

    • Author(s)
      Ishizawa, J., Yoshida S., Oya, M., Mizuno, R., Shinojima, T., Marumo, K., Murai, M.
    • Journal Title

      International Journal of Oncology 25

      Pages: 697-702

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Differential expression of activator protein-2 isoforms in renal cell carcinoma.2004

    • Author(s)
      Oya, M.et al.
    • Journal Title

      Urology 64

      Pages: 162-167

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Inhibition of MKP-1 expression potentiates JNK related apoptosis in renal cancer cells.2004

    • Author(s)
      Mizuno, R., Oya, M.et al.
    • Journal Title

      J.Urol. 172

      Pages: 723-727

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Dexamethasone and interleukin-2 combination therapy for advanced renal cell carcinoma in a patient with paraneoplastic syndrome.2004

    • Author(s)
      Shinojima, T., Oya M.et al.
    • Journal Title

      Int.J.Urol. 11

      Pages: 553-556

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Inhibition of the ubiquitin-proteasome pathway activates stress kinases and induces apoptosis in renal cancer cells.2004

    • Author(s)
      Ishizawa, J., Yoshida S., Oya, M.et al.
    • Journal Title

      Int.J.Oncol. 25

      Pages: 697-702

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Renal cell carcinoma : etiology, incidence and epidemiology.2004

    • Author(s)
      Murai, M., Oya, M.
    • Journal Title

      Curr.Opin.Urol. 14

      Pages: 229-233

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Increased nuclear factor-κB activation is related to the tumor development of renal cell carcinoma.2003

    • Author(s)
      Oya, M., Takayanagi, A., Horiguchi, A., Mizuno, R., Ohtsubo, M., Marumo, K., Shimizu, N., Murai, M.
    • Journal Title

      Carcinogenesis 24

      Pages: 377-384

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Increased activation of CCAAT/enhancer binding protein-β correlates with the invasiveness of renal cell carcinoma.2003

    • Author(s)
      Oya, M., Horiguchi, A., Mizuno, M., Marumo, K., Murai, M.
    • Journal Title

      Clinical Cancer Research 9

      Pages: 1021-1027

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Elevated AKT activation and its impact on clinicopathological features of renal cell carcinoma.2003

    • Author(s)
      Horiguchi, A., Oya, M., Shimada, T., Uchida, A., Marumo, K., Murai, M
    • Journal Title

      Journal of Urology 169

      Pages: 710-713

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Publications] Oya M, Takayanagi A, Horiguchi A, Mizuno M, Ohtsubo M, Marumo K, Shimizu N, Murai M.: "Increased nuclear factor-κB activation is related to the tumor development of renal cell carcinoma."Carcinogenesis. 24・3. 377-384 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Oya M, Horiguchi A, Mizuno M, Marumo K, Murai M.: "Increased activation of CCAAT/enhancer binding protein-β correlates with the invasiveness of renal cell carcinoma."Clinical Cancer Research. 19・3. 1021-1027 (2003)

    • Related Report
      2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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