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Elucidation of the role of Interleukin-32 involved in the invasive process of pancreatic cancer and its expression mechanism.

Research Project

Project/Area Number 16K08707
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Experimental pathology
Research InstitutionUniversity of Toyama

Principal Investigator

Imura Johji  富山大学, 大学院医学薬学研究部(医学), 教授 (80316554)

Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords膵癌 / 浸潤 / IL-32 / 細胞株 / Interleukin-32 / サイトカイン
Outline of Final Research Achievements

This study was performed to investigate the invasiveness regulating factors that defines poor prognosis for pancreatic cancer. First, a highly invasive cell was established from the human-derived pancreatic cancer cell lines. IL-32 has been highly enhanced among several genes to expression. Furthermore it was confirmed whether IL-32 was involved in invasiveness. It was found that the invasiveness was inhibited by siRNA for IL-32, and the invasiveness was obtained when IL-32 was forcibly expressed in non-invasive cell. In pancreatic cancer tissues, the expression of IL-32 was not appeared in normal pancreatic ducts, was expressed in tumor cells, and it was particularly enhanced in the infiltrating area. The factors regulated by IL-32 were involved E-Cadherin, MMP4・14・9, Thrombospondin 1, Slug, BMP4 and etc.
From the above, it was suggested that IL-32 may be an important factor involved not only in inflammation but also in the invasiveness of pancreatic cancer.

Academic Significance and Societal Importance of the Research Achievements

膵癌は最近、死亡率が増加の一途を辿っている。何故に、膵癌が予後不良なのか?その原因は数々あるが、特に膵癌は容易に周辺臓器に浸潤し易く、手術不能となることも要因である。では、なぜに易浸潤性なのか?浸潤を制御している機構や分子はどの様なものがあるのか?それらを明らかにすることが本研究の目的である。まず、浸潤性の高い細胞を作成し、これらで高発現している分子の中からL-32を見出した。さらに、IL-32を減少させると浸潤性が減弱し、亢進させると浸潤性を増すことを確認した。また、IL-32によって制御を受ける分子も明らかにした。今後、IL-32と共に、他の分子を抑制するような創薬にも繋がる研究である。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (12 results)

All 2019 2018 2017 2016

All Journal Article (3 results) (of which Peer Reviewed: 3 results,  Open Access: 3 results) Presentation (9 results)

  • [Journal Article] Bile cytology: A new scoring system for improving diagnostic accuracy.2019

    • Author(s)
      Hayakawa C, Hoshikawa M, Imura J, Ueno T, Koike J
    • Journal Title

      Diagn Cytopathol

      Volume: 2019 Issue: 7 Pages: 1-7

    • DOI

      10.1002/dc.24076

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Endoglin (CD105) and SMAD4 regulate spheroid formation and the suppression of the invasive ability of human pancreatic cancer cells.2018

    • Author(s)
      Kokaji E, Shimomura A, Minamisaka T, Nakajima T, Miwa S, Hatta H, Nishida T, Kiya C, Imura J
    • Journal Title

      Int J Oncol

      Volume: 52 Pages: 892-900

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] SKL2001 suppresses colon cancer spheroid growth through regulation of the E-cadherin/β-Catenin complex.2018

    • Author(s)
      Ohashi W, Yamamine N, Imura J, Hattori Y.
    • Journal Title

      Biochem Biophys Res Commun

      Volume: 493 Pages: 1342-1348

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed / Open Access
  • [Presentation] Exprolatory study for regulatory molecules expressed in pancreatic cancer cell lines showing various behaviors2018

    • Author(s)
      井村 穣二、下村 明子, 高木 康司, 川口 真一, 南坂 尚, 中嶋 隆彦, 西田 健志, 八田 秀樹
    • Organizer
      第77回癌学会総会
    • Related Report
      2018 Annual Research Report
  • [Presentation] 高浸潤性膵癌細胞株から樹立化され異なった挙動を示すサブクローン化細胞内で発現する分子の探索2018

    • Author(s)
      井村 穣二、下村 明子, 高木 康司, 川口 真一, 南坂 尚, 中嶋 隆彦, 西田 健志, 八田 秀樹
    • Organizer
      第107回日本病理学会総会
    • Related Report
      2018 Annual Research Report
  • [Presentation] 膵癌の浸潤にはIL-32 が関与する2017

    • Author(s)
      井村 穣二
    • Organizer
      第106回 日本病理学会総会
    • Place of Presentation
      東京
    • Year and Date
      2017-04-27
    • Related Report
      2016 Research-status Report
  • [Presentation] IL-32は膵癌における腫瘍細胞の浸潤を制御する2017

    • Author(s)
      井村 穣二, 高木 康司, 下村 明子, 小梶 恵利, 南坂 尚, 三輪 重治, 中嶋 隆彦
    • Organizer
      第76回日本癌学会
    • Related Report
      2017 Research-status Report
  • [Presentation] ヒト膵癌細胞株のspheroid形成におけるSMAD4及びendoglinの関与2017

    • Author(s)
      小梶 恵利, 井村 穣二
    • Organizer
      第76回日本癌学会
    • Related Report
      2017 Research-status Report
  • [Presentation] 膵癌細胞株のspheroid形成におけるSMAD4の発現動態とその機能に関する検討2017

    • Author(s)
      小梶 恵利, 西田 健志, 下村 明子, 南坂 尚, 中嶋 隆彦, 三輪 重治, 林 伸一, 井村 穣二
    • Organizer
      第106回日本病理学会総会
    • Related Report
      2017 Research-status Report
  • [Presentation] 膵癌の浸潤にはIL-32が関与する2017

    • Author(s)
      井村 穣二, 高木 康司, 下村 明子, 南坂 尚, 中嶋 隆彦, 三輪 重治, 林 伸一, 西田 健志, 八田 秀樹
    • Organizer
      第106回日本病理学会総会
    • Related Report
      2017 Research-status Report
  • [Presentation] IL-32 controls the invasive ability of the pancreatic cancer cells2016

    • Author(s)
      井村 穣二
    • Organizer
      第75回日本癌学会学術総会
    • Place of Presentation
      横浜
    • Year and Date
      2016-10-06
    • Related Report
      2016 Research-status Report
  • [Presentation] 膵癌における浸潤機構の解明ーinterleukin-32の関わり2016

    • Author(s)
      井村 穣二
    • Organizer
      第27回日本消化器癌発生学会総会
    • Place of Presentation
      鹿児島
    • Year and Date
      2016-09-15
    • Related Report
      2016 Research-status Report

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Published: 2016-04-21   Modified: 2021-02-19  

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