MiR-526b-3p Inhibits the Resistance of Glioma Cells to Adriamycin by Targeting MAPRE1
Background. Cell resistance is the main reason for the high mortality in glioma. Adriamycin (ADR) is a treatment drug for glioma and often leads to chemoresistance. Previous studies have confirmed that the abnormal expression of microRNA (miRNA) affects the resistance of glioma cells. Methods. RT-qP...
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Veröffentlicht in: | Journal of oncology 2022-02, Vol.2022, p.2402212-13 |
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Sprache: | eng |
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Zusammenfassung: | Background. Cell resistance is the main reason for the high mortality in glioma. Adriamycin (ADR) is a treatment drug for glioma and often leads to chemoresistance. Previous studies have confirmed that the abnormal expression of microRNA (miRNA) affects the resistance of glioma cells. Methods. RT-qPCR and western blot were conducted for detecting miR-526b-3p levels and related protein expressions. CCK8 assay, colony formation, flow cytometry, and Transwell were adopted to assess cell viability, proliferation, apoptosis, and metastasis. Moreover, downstream targets of miR-526b-3p were identified through a dual-luciferase reporter and RNA pull-down analysis. Results. Nevertheless, miR-526b-3p functions on glioma cell resistance to ADR are not well characterized. This study demonstrated that miR-526b-3p levels were decreased within glioma cells and further decreased within ADR-resistant glioma cells. Then, miR-526b-3p overexpression repressed glioma cell proliferation and invasion while inducing cell apoptosis. Overexpression of miR-526b-3p within ADR-resistant glioma cells obtained similar results, which suggested miR-526b-3p suppressed glioma cell resistance to ADR. Mechanistically, miR-526b-3p targeted MAPKE1 and negatively regulated MAPKE1 expressions. Restoration of MAPKE1 levels reversed miR-526b-3p effects on the glioma process and resistance to ADR. Conclusion. These results suggest that miR-526b-3p acts as a diagnostic marker in glioma development and therapeutic target of the glioma resistance to ADR. |
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ISSN: | 1687-8450 1687-8450 |
DOI: | 10.1155/2022/2402212 |