4.7 Article

Inhalational Anesthetics Inhibit Neuroglioma Cell Proliferation and Migration via miR-138,-210 and-335

Journal

Publisher

MDPI
DOI: 10.3390/ijms22094355

Keywords

microRNA; sevoflurane; desflurane; hypoxia inducible factor-1α matrix metalloproteinase 9; glioma

Funding

  1. ONO PHARMACEUTICAL CO., LTD., Osaka, Japan [ONOS20190517001]
  2. BOC Chair grant, Royal College of Anaesthetists, London, UK

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Inhalational anesthetics sevoflurane and desflurane were found to inhibit glioma cell malignancy through upregulation of miRNAs and downregulation of their downstream effectors HIF-1 alpha and MMP9. Further studies are warranted to explore the implications of these findings.
Inhalational anesthetics was previously reported to suppress glioma cell malignancy but underlying mechanisms remain unclear. The present study aims to investigate the effects of sevoflurane and desflurane on glioma cell malignancy changes via microRNA (miRNA) modulation. The cultured H4 cells were exposed to 3.6% sevoflurane or 10.3% desflurane for 2 h. The miR-138, -210 and -335 expression were determined with qRT-PCR. Cell proliferation and migration were assessed with wound healing assay, Ki67 staining and cell count kit 8 (CCK8) assay with/without miR-138/-210/-335 inhibitor transfections. The miRNA downstream proteins, hypoxia inducible factor-1 alpha (HIF-1 alpha) and matrix metalloproteinase 9 (MMP9), were also determined with immunofluorescent staining. Sevoflurane and desflurane exposure to glioma cells inhibited their proliferation and migration. Sevoflurane exposure increased miR-210 expression whereas desflurane exposure upregulated both miR-138 and miR-335 expressions. The administration of inhibitor of miR-138, -210 or -335 inhibited the suppressing effects of sevoflurane or desflurane on cell proliferation and migration, in line with the HIF-1 alpha and MMP9 expression changes. These data indicated that inhalational anesthetics, sevoflurane and desflurane, inhibited glioma cell malignancy via miRNAs upregulation and their downstream effectors, HIF-1 alpha and MMP9, downregulation. The implication of the current study warrants further study.

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