MicroRNA‑574 inhibits cell proliferation and invasion in glioblastoma multiforme by directly targeting zinc finger E‑box‑binding homeobox 1.

Abstract

Accumulated evidence has demonstrated that dysregulation of microRNAs (miRNAs) contributes to tumourigenesis and tumour development of glioblastoma multiforme (GBM). Therefore, miRNAs may be promising candidates in the development of prognosis biomarkers and effective therapeutic targets for patients with GBM. A number of studies have reported that miRNA‑574 (miR‑574) is aberrantly expressed in multiple types of human cancers. However, the expression pattern, biological functions and molecular mechanism of miR‑574 in GBM are yet to be elucidated. Therefore, the present study aimed to determine the expression level and biological functions of miR‑574 in GBM and the underlying molecular mechanisms. In the present study, miR‑574 levels were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and were demonstrated to be significantly downregulated in human GBM tissues and cell lines. Functional experiments indicated that restored expression of miR‑574 using mimics led to the inhibition of the cell proliferation and invasion of GBM cells, as determined by Cell Counting kit‑8 and Matrigel invasion assays, respectively. In addition, bioinformatics analysis predicted that zinc finger E‑box‑binding homeobox1 (ZEB1) may be a target of miR‑574. Subsequent RT‑qPCR, western blot analysis and luciferase reporter assays confirmed that ZEB1 was a direct target of miR‑574 in GBM. Additionally, ZEB1 was demonstrated to be upregulated and inversely correlated with miR‑574 expression in clinical GBM tissues. Rescue experiments demonstrated that overexpression of ZEB1 attenuated the inhibitory effects of miR‑574 on the proliferation and invasion of GBM cells. Overall, the results of the present study highlighted the potential tumour inhibitory roles of miR‑574 in GBM, thereby indicating that miR‑574 may be a novel and efficient therapeutic target for the treatment of patients with GBM.