MiR‑493‑5p inhibits the malignant development of gliomas via suppressing E2F3‑mediated dysfunctions of P53 and PI3K/AKT pathways

• Hong Liu ^[1] ; Zhen Li ^[2] ; Hu Sun ^[3]
  1. [1] Department of Oncology, Binzhou Center Hospital, Shandong 251700, China
  2. [2] Department of Neurosurgery, LinYi People’s Hospital, Shandong, China
  3. [3] Department of Neurosurgery, Zibo Central Hospital, No. 54 West Communist Youth League Road, Shandong 255000, China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 24, Nº. 2, 2022, págs. 363-370
• Idioma: inglés
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• Resumen

  • Background Gliomas is a major challenge of current medical system, and thousands of people are struggling in the pain of this disease worldwide. In the last decade, the functions of miRNAs have been revealed by many studies, and the interven- tion on miRNA dysfunctions has been thought as a promising way to counter cancer. MiR-493-5p has been identified as a tumor inhibitor to suppress the progressions of several tumors while its role in gliomas remains unknown. Hence, the study investigated the expression levels of miR-493-5p in glioma tissues and cell lines.

    Methods CCK-8 assay, transwell assay and flow cytometry assay were used to observe the effects of miR-493-5p on tumor cells. The downstream targets of miR-493-5p were also searched and verified with online databases and dual-luciferase reporter assay. Moreover, the activities of P53 and PI3K/AKT pathways were also explored by western blot to illustrate the regulation mechanism of miR-493-5p on glioma development.

    Results The results showed that miR-493-5p was significantly downregulated in pathological tissues and glioma cell lines, and the increased miR-493-5p effectively inhibited the malignant behavior and promoted the apoptosis of glioma cells.

    Conclusions E2F3 was confirmed as a target of miR-493-5p, and the effects of miR-493-5p on the phenotype of glioma cells could be partly reversed by E2F3. Besides, it was also found that miR-493-5p could effectively suppress the expression of E2F3 and then improve the dysfunctions of the P53 and PI3K/AKT pathways.