MicroRNA‑566 modulates vascular endothelial growth factor by targeting Von Hippel‑Landau in human glioblastoma in vitro and in vivo.

MicroRNAs (miRNAs) are able to function as either oncogenes or tumor suppressor genes in tumorigenesis, and have been proposed as novel targets for anticancer treatment. It has previously been suggested that miRNAs have important roles in the initiation and progression of glioblastoma; however, the effects of miR‑566 in glioblastoma are currently unclear. The present study aimed to demonstrate that miR-566 can modulate vascular endothelial growth factor (VEGF) by targeting Von Hippel‑Lindau (VHL) in glioblastoma in vitro and in vivo by inhibiting the expression of miR-566. Glioblastoma is a highly vascularized tumor, which exhibits increased expression of angiogenic factors, including VEGF, which are crucial in the process of glioblastoma angiogenesis. Existing research has demonstrated that VHL is a tumor suppressor gene that is associated with various tumors. In addition, VHL is able to regulate the expression of VEGF by promoting the degradation of hypoxia‑inducible factor‑1α via ubiquitination. It has been predicted, using bioinformatics, that the VHL gene is regulated by miR‑566. Therefore, the present study hypothesized that miR‑566 may regulate VEGF expression by targeting VHL during the angiogenic process of glioblastoma multiforme. The results of the present study demonstrated that inhibition of miR‑566 expression increases the expression levels of VHL, decreases the expression levels of VEGF, and inhibits the invasive and migratory abilities of glioblastoma. In addition, VHL was identified as a functional target of miR‑566.