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Immature Schwann cells contribute to pancreatic cancer cell migration and invasion

Research Project

Project/Area Number 18K07382
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 51030:Pathophysiologic neuroscience-related
Research InstitutionOsaka University

Principal Investigator

Suzuki Masami  大阪大学, 医学系研究科, 助教 (80434182)

Project Period (FY) 2018-04-01 – 2021-03-31
Project Status Completed (Fiscal Year 2020)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywordsがん / シュワン細胞 / がん細胞 / クロストーク
Outline of Final Research Achievements

The nerve repair signaling following nerve injury may facilitates cancer progression. I previously revealed that Schwann cells were dedifferentiated into immature Schwann cells by cancer cells-induced peripheral nerve injury. In this study, I investigated the role of immature Schwann cells in cancer cells migration/invasion. Conditioned medium from immature Schwann cells significantly enhanced the migration of cancer cells toward the conditioned medium. To explore the collaboration between immature Schwann cells and cancer cells, we developed in vitro coculture system. Immature Schwann cells was associated with cancer cells with their protrusions and formed tunnels. These results suggest that immature Schwann cells dedifferentiated by cancer cells might be a key regulator of cancer cell migration and invasion.

Academic Significance and Societal Importance of the Research Achievements

これまでのがん研究は、発生学や免疫学からのアプローチが主で、神経科学的にアプローチされることは少なかった。本研究の学術的意義は、がんにより引き起こされる神経障害、特にシュワン細胞の脱分化により誘導された未分化型のシュワン細胞が、がん細胞の遊走能および浸潤能を増大させることを明らかにした点である。本研究成果は、がんによる神経障害を制御することががんの進展を抑制することを示唆しており、これら重複する分子メカニズムをターゲットとした治療は、神経障害に伴う難治性の痛みを軽減するだけではなく、がんの増悪を抑制できる可能性が考えられる。

Report

(4 results)
  • 2020 Annual Research Report   Final Research Report ( PDF )
  • 2019 Research-status Report
  • 2018 Research-status Report
  • Research Products

    (3 results)

All 2020 2019 2018

All Journal Article (3 results) (of which Peer Reviewed: 3 results,  Open Access: 2 results)

  • [Journal Article] E74-Like Factor 3 Is a Key Regulator of Epithelial Integrity and Immune Response Genes in Biliary Tract Cancer2020

    • Author(s)
      Suzuki Masami、Saito-Adachi Mihoko、Arai Yasuhito、Fujiwara Yuko、Takai Erina、Shibata Shinsuke、Seki Masahide、Rokutan Hirofumi、Maeda Daichi、Horie Masafumi、Suzuki Yutaka、Shibata Tatsuhiro、Kiyono Tohru、Yachida Shinichi
    • Journal Title

      Cancer Research

      Volume: 81 Issue: 2 Pages: 489-500

    • DOI

      10.1158/0008-5472.can-19-2988

    • Related Report
      2020 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Carboplatin Enhances the Activity of Human Transient Receptor Potential Ankyrin 1 Through the Cyclic AMP-Protein Kinase A-A-Kinase Anchoring Protein (AKAP) Pathways2019

    • Author(s)
      Miyano K, Shiraishi S, Minami K, Sudo Y, Suzuki M, Yokoyama T, Terawaki K, Nonaka M, Murata H, Higami Y, Uezono Y.
    • Journal Title

      Int J Mol Sci

      Volume: 13 Pages: 3271-3271

    • Related Report
      2019 Research-status Report
    • Peer Reviewed
  • [Journal Article] Establishment of preclinical chemotherapy models for gastroenteropancreatic neuroendocrine carcinoma2018

    • Author(s)
      Ohmoto A, Suzuki M, Takai E, Routan H, Fujiwara Y, Morizane C, Yanagihara K, Shibata T, Yachida S
    • Journal Title

      Oncotarget

      Volume: 30 Issue: 30 Pages: 21086-21099

    • DOI

      10.18632/oncotarget.24930

    • Related Report
      2018 Research-status Report
    • Peer Reviewed / Open Access

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Published: 2018-04-23   Modified: 2022-01-27  

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