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Functional Analysis of Apoptosis Regulatory Factor GRIM19 in Oral Carcinoma Cells

Research Project

Project/Area Number 25462929
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pathobiological dentistry/Dental radiology
Research InstitutionMeikai University

Principal Investigator

Mori Kazumasa  明海大学, 歯学部, 講師 (80372902)

Co-Investigator(Kenkyū-buntansha) Yoshihiro Ohmori  明海大学, 歯学部, 教授 (50194311)
Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
KeywordsGRIM19 / 扁平上皮癌 / アポトーシス / IFN / オートファジー / STAT3 / GRIM-19 / IFN / Lactacystin / rapamycin
Outline of Final Research Achievements

We have investigated the expression of the GRIM-19 in oral squamous cell carcinoma cell lines and found a low-GRIM-19 expression cell line (HSC-2) and a high- GRIM-19 expression cell line (Ca9-22). Our results also suggested that the expression of the GRIM-19 is regulated at the protein levels but not transcriptional level. To determine the regulatory mechanism for the expression of GRIM-19 protein, we analyzed the involvement of ubiquitin-proteasome systems and autophagy system using various inhibitors. The results demonstrated that the expression of GRIM-19 protein unregulated by treatment with the proteasome and the autophagy inhibitors in Ca9-22 cells. However neither the proteasome inhibitor nor the autophagy inhibitor enhanced the expression in HSC-2 cells. These results suggest a possibility that the impaired expression of GRIM-19 in HSC-2 cells is due to a mutation in the cording region of the GRIM-19 gene.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report
  • Research Products

    (3 results)

All 2015 2014

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results,  Acknowledgement Compliant: 1 results) Presentation (2 results)

  • [Journal Article] Tumor-associated macrophages in oral premalignant lesions coexpress CD163 and STAT1 in a Th1-dominated microenvironment.2015

    • Author(s)
      Kazumasa Mori, Shigeki Haragchi, Miki Hiroi, Yoshihiro Ohmori
    • Journal Title

      BMC Cancer

      Volume: 15 Issue: 1

    • DOI

      10.1186/s12885-015-1587-0

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Presentation] 口腔癌細胞におけるアポトーシス制御因子GRIM19の発現制御機構2014

    • Author(s)
      森 一将
    • Organizer
      第59回 公益社団法人 日本口腔外科学会総会・学術大会
    • Place of Presentation
      千葉県 千葉市 幕張メッセ国際会議場
    • Year and Date
      2014-10-17 – 2014-10-19
    • Related Report
      2014 Research-status Report
  • [Presentation] 口腔癌細胞におけるアポトーシス制御因子GRIM19の発現制御機構2014

    • Author(s)
      森 一将
    • Organizer
      第56回歯科基礎医学会学術大会・総会
    • Place of Presentation
      福岡県 福岡市 福岡国際会議場
    • Year and Date
      2014-09-24 – 2014-09-27
    • Related Report
      2014 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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