Identification and functional analysis of an EMT-accelerating factor induced in pancreatic cancer cells by an anticancer agent

  • SHIMASAKI Takeo
    Medical Research Institute, Kanazawa Medical University Project Research Center, Kanazawa Medical University Department of Gastroenterology, Kanazawa Medical University
  • YAMAMOTO Satoko
    Medical Research Institute, Kanazawa Medical University
  • ISHIGAKI Yasuhito
    Medical Research Institute, Kanazawa Medical University
  • TAKATA Takanobu
    Medical Research Institute, Kanazawa Medical University
  • ARISAWA Tomiyasu
    Department of Gastroenterology, Kanazawa Medical University
  • MOTOO Yoshiharu
    Department of Medical Oncology, Kanazawa Medical University
  • TOMOSUGI Naohisa
    Medical Research Institute, Kanazawa Medical University Project Research Center, Kanazawa Medical University
  • MINAMOTO Toshinari
    Division of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University

Bibliographic Information

Other Title
  • 抗がん剤により膵癌細胞に誘導されるEMT促進因子の同定と機能解析

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Abstract

Pancreatic cancer leads to increased proliferation, invasion, resistance to anticancer agents and radiation, and metastasis. The epithelial-to-mesenchymal transition (EMT) is a characteristic known to be involved during the progression of cancer cells. We found that gemcitabine (GEM) triggers EMT-like changes of pancreatic cancer. To investigate the molecular mechanism of GEM-induced EMT in cancer cells, we analyzed proteome profiles of cell culture medium to identify proteins that may potentially induce EMT in PANC-1 cells in response to GEM. Following the treatment with GEM, various proteins in the medium were decreased, whereas, heat shock protein 90 (HSP90) was mostly increased. Recombinant HSP90 protein induced morphological changes and EMT-related markers in cancer cells. These results indicate that excretory HSP90 is responsible for GEM-induced EMT in cancer cells and suggest the necessity to establish a therapeutic strategy for preventing such unwanted biological effects induced by chemotherapeutics in pancreatic cancer cells.

Journal

  • Suizo

    Suizo 31 (1), 76-84, 2016

    Japan Pancreas Society

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