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Analysis of the molecular pathology of frequently-accompanied pulmonary cancer in fibrotic lung

Research Project

Project/Area Number 26860185
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General medical chemistry
Research InstitutionTokyo Medical and Dental University

Principal Investigator

Maruyama Junichi  東京医科歯科大学, 大学院医歯学総合研究科, 助教 (30723639)

Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords肺線維症 / 肺癌 / DNA損傷修復 / 癌転移
Outline of Final Research Achievements

The molecular mechanism how idiopathic pulmonary fibrosis (IPF) is often accompanied by lung cancer is not fully understood. To address this question, I re-analyzed the GEO gene expression data obtained from IPF lung samples and identified DCLK1 as an up-regulated gene in the IPF lung. DCLK1 has been reported as a marker gene of cancer stem cells. I revealed that DCLK1 suppresses the activity of DNA repairing system and that DCLK1 protein expression level is up-regulated by the treatment of macrophage-like cell-conditioned medium. Taken together, it is suggested that the up-regulation of DCLK1 protein amount in the lung facilitates tumorigenesis and that this up-regulation can be promoted by the accumulation of macrophage cells in the lung.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report
  • Research Products

    (7 results)

All 2017 2016 2015 2014

All Journal Article (6 results) (of which Int'l Joint Research: 4 results,  Peer Reviewed: 6 results,  Open Access: 5 results,  Acknowledgement Compliant: 4 results) Presentation (1 results)

  • [Journal Article] Domain analysis of Ras-association domain family member 6 upon interaction with MDM2.2017

    • Author(s)
      Sarkar A, Iwasa H, Hossain S, Xu X, Sawada T, Shimizu T, Maruyama J, Arimoto-Matsuzaki K, Hata Y.
    • Journal Title

      FEBS Letters

      Volume: 591 Issue: 2 Pages: 260-272

    • DOI

      10.1002/1873-3468.12551

    • Related Report
      2016 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] Validation of the chemical compound library screening for TAZ inhibitors by use of green fluorescence protein-fused TAZ.2016

    • Author(s)
      Nagashima S, Maruyama J, Kawano S, Iwasa H, Nakagawa K, Ishigami-Yuasa M, Kagechika H, Nishina H, Hata Y.
    • Journal Title

      Cancer Sci.

      Volume: - Issue: 6 Pages: 791-802

    • DOI

      10.1111/cas.12936

    • Related Report
      2016 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] Osmotic stress induces the phosphorylation of WNK4 Ser575 via the p38MAPK-MK pathway.2016

    • Author(s)
      Maruyama J, Kobayashi Y, Umeda T, Vandewalle A, Takeda K, Ichijo H, Naguro I.
    • Journal Title

      Sci. Rep.

      Volume: 6 Issue: 1 Pages: 18710-18710

    • DOI

      10.1038/srep18710

    • NAID

      120006987229

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] A cell-based screening for TAZ activators identifies ethacridine, a widely used antiseptic and abortifacient, as a compound that promotes dephosphorylation of TAZ and inhibits adipogenesis in C3H10T1/2 cells.2015

    • Author(s)
      Kawano S, Maruyama J, Nagashima S, Inami K, Qiu W, Iwasa H, Nakagawa K, Ishigami-Yuasa M, Kagechika H, Nishina H, Hata Y.
    • Journal Title

      J. Biochem.

      Volume: 158 Issue: 5 Pages: 413-423

    • DOI

      10.1093/jb/mvv051

    • NAID

      40020646985

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] A new cell-based assay to evaluate myogenesis in mouse myoblast C2C12 cells2015

    • Author(s)
      Kodaka, M.; Yang, Z.; Nakagawa, K.; Maruyama, J.; Xu, X.; Sarkar, A.; Ichimura, A.; Nasu, Y.; Ozawa, T.; Iwasa, H.; Ishigami-Yuasa, M.; Ito, S.; Kagechika, H.; Hata, Y.
    • Journal Title

      Exp. Cell. Res.

      Volume: 336 Issue: 2 Pages: 171-181

    • DOI

      10.1016/j.yexcr.2015.06.015

    • Related Report
      2015 Research-status Report
    • Peer Reviewed
  • [Journal Article] Screening with a Novel Cell-Based Assay for TAZ Activators Identifies a Compound That Enhances Myogenesis in C2C12 Cells and Facilitates Muscle Repair in a Muscle Injury Model.2014

    • Author(s)
      Yang, Z. Y.; Nakagawa, K.; Sarkar, A.; Maruyama, J.; Iwasa, H.; Bao, Y. J.; Ishigami-Yuasa, M.; Ito, S.; Kagechika, H.; Hata, S.; Nishina, H.; Abe, S.; Kitagawa, M.; Hata, Y.
    • Journal Title

      Mol. Cell. Biol.

      Volume: 34 Issue: 9 Pages: 1607-1621

    • DOI

      10.1128/mcb.01346-13

    • Related Report
      2014 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] 新規に同定したYAP1活性化化合物は多発性骨髄腫細胞においてYAP1-p73経路依存的な細胞死を誘導する2016

    • Author(s)
      丸山 順一、江 欣亮、岩佐 宏晃、湯浅(石上) 磨里、影近 弘之、仁科 博史、畑 裕
    • Organizer
      第39回日本分子生物学会年会
    • Place of Presentation
      パシフィコ横浜、神奈川県横浜市
    • Year and Date
      2016-11-30
    • Related Report
      2016 Annual Research Report

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Published: 2014-04-04   Modified: 2018-03-22  

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