Dexmedetomidine promotes tumorigenicity via circular RNA BRAF/microRNA-381-3p /thrombospondin 2 in glioma
By: Cai, Lisong
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Contributor(s): Yajing, Zheng.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2023Edition: Vol.85(3), May-Jul.Description: 721-731p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: Glioma is the most frequent primary intracranial tumor worldwide. Dexmedetomidine is an efficient anesthetic used in surgery and has an impact on glioma. Yet, the mechanism of dexmedetomidine on the biological characteristics of glioma cells is unknown. Circ_BRAF, microRNA-381-3p and thrombospondin 2 was detected via quantitative reverse transcription-polymer chine reaction. Proliferation detection was conducted using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Transwell assay was used to determine cell migratory and invasive capacities. The protein expression was determined using Western blot. Binding between microRNA- 381-3p and circ_BRAF or thrombospondin 2 was validated using dual-luciferase reporter. Role between dexmedetomidine and circ_BRAF on glioma growth was analyzed using the xenograft tumor model in mice. Dexmedetomidine inhibited circ_BRAF expression in glioma cells in a dose-dependent manner. Dexmedetomidine induced glioma cell proliferation, migration and invasion was neutralized via circ_ BRAF up regulation. Meanwhile, circ_BRAF could facilitate thrombospondin 2 expression via binding with miR-381-3p. Besides, dexmedetomidine was revealed to promote glioma tumourogenesis in vivo via circ_BRAF/ microRNA-381-3p/thrombospondin 2 pathways. Dexmedetomidine exposure expedited glioma development via circ_BRAF/microRNA-381-3p/thrombospondin 2 axis, providing a theoretical basis for glioma therapy.
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School of Pharmacy Archieval Section | Not for loan | 2024-0207 |
Glioma is the most frequent primary intracranial tumor worldwide. Dexmedetomidine is an efficient anesthetic used in surgery and has an impact on glioma. Yet, the mechanism of dexmedetomidine on the biological characteristics of glioma cells is unknown. Circ_BRAF, microRNA-381-3p and thrombospondin 2 was detected via quantitative reverse transcription-polymer chine reaction. Proliferation detection was conducted using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Transwell assay was used to determine cell migratory and invasive capacities. The protein expression was determined using Western blot. Binding between microRNA- 381-3p and circ_BRAF or thrombospondin 2 was validated using dual-luciferase reporter. Role between dexmedetomidine and circ_BRAF on glioma growth was analyzed using the xenograft tumor model in mice. Dexmedetomidine inhibited circ_BRAF expression in glioma cells in a dose-dependent manner. Dexmedetomidine induced glioma cell proliferation, migration and invasion was neutralized via circ_ BRAF up regulation. Meanwhile, circ_BRAF could facilitate thrombospondin 2 expression via binding with miR-381-3p. Besides, dexmedetomidine was revealed to promote glioma tumourogenesis in vivo via circ_BRAF/ microRNA-381-3p/thrombospondin 2 pathways. Dexmedetomidine exposure expedited glioma development via circ_BRAF/microRNA-381-3p/thrombospondin 2 axis, providing a theoretical basis for glioma therapy.
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