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Article

Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells

  • Authors:
    • Naotoshi Sugimoto
    • Hiroaki Ishibashi
    • Hiroyuki Nakamura
    • Akihiro Yachie
    • Takako Ohno-Shosaku
  • View Affiliations / Copyright

    Affiliations: Department of Physiology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa 920‑8640, Japan, Department of Oral and Maxillofacial Surgery, Kanazawa Medical University, Uchinada 920‑0293, Japan, Department of Public Health Pediatrics, Graduate School of Medical Sciences, Kanazawa University, Kanazawa 920‑8640, Japan, Department of Pediatrics, Graduate School of Medical Sciences, Kanazawa University, Kanazawa 920‑8640, Japan, Impairment Study, Graduate School of Medical Sciences, Kanazawa University, Kanazawa 920-0942, Japan
  • Pages: 3702-3708
    |
    Published online on: October 20, 2017
       https://doi.org/10.3892/or.2017.6048
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Abstract

The endocannabinoid system plays an important role in the regulation of physiological and pathological conditions, including inflammation and cancer. Hypoxia is a fundamental phenomenon for the establishment and maintenance of the microenvironments in various physiological and pathological conditions. However, the influence of hypoxia on the endocannabinoid system is not fully understood. In the present study, we investigated the effects of hypoxia on the endocannabinoid system in malignant brain tumors. We subjected U-87 MG cells, derived from malignant glioblastoma, to hypoxia (1.5% O2) for 3 days, and evaluated their viability and expression of endocannabinoid-related genes. Hypoxia decreased the expression of cannabinoid receptor 1 and the astrocyte marker glial fibrillary acidic protein, and increased the expression of vascular endothelial growth factor and cyclooxygenase-2, the enzyme responsible for the metabolism of endocannabinoids, in U-87 MG cells. Although cannabinoid receptor (CB) engagement induces cell death in U-87 MG cells in normoxic conditions, CB agonist-induced death was attenuated in hypoxic conditions. These results suggest that hypoxia modifies the endocannabinoid system in glioblastoma cells. Hypoxia-induced inhibition of the endocannabinoid system may aid the development of glioblastoma.
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Copy and paste a formatted citation
Spandidos Publications style
Sugimoto N, Ishibashi H, Nakamura H, Yachie A and Ohno-Shosaku T: Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells. Oncol Rep 38: 3702-3708, 2017.
APA
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., & Ohno-Shosaku, T. (2017). Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells. Oncology Reports, 38, 3702-3708. https://doi.org/10.3892/or.2017.6048
MLA
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., Ohno-Shosaku, T."Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells". Oncology Reports 38.6 (2017): 3702-3708.
Chicago
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., Ohno-Shosaku, T."Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells". Oncology Reports 38, no. 6 (2017): 3702-3708. https://doi.org/10.3892/or.2017.6048
Copy and paste a formatted citation
x
Spandidos Publications style
Sugimoto N, Ishibashi H, Nakamura H, Yachie A and Ohno-Shosaku T: Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells. Oncol Rep 38: 3702-3708, 2017.
APA
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., & Ohno-Shosaku, T. (2017). Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells. Oncology Reports, 38, 3702-3708. https://doi.org/10.3892/or.2017.6048
MLA
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., Ohno-Shosaku, T."Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells". Oncology Reports 38.6 (2017): 3702-3708.
Chicago
Sugimoto, N., Ishibashi, H., Nakamura, H., Yachie, A., Ohno-Shosaku, T."Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells". Oncology Reports 38, no. 6 (2017): 3702-3708. https://doi.org/10.3892/or.2017.6048
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