MicroRNAs are important regulators of multiple cellular processes, and aberrant miRNA expression has been observed in human glioblastoma (GBM). The present study was to evaluate the level of miR-124 and signal transducer and activator of transcription 3 (STAT3) in GBM tissues and cells. We further investigated the molecular mechanisms of miR-124 and STAT3 in GBM cell lines U87 and U251. Here, we found that miR-124 expression was downregulated in GBM tissues and U87 and U251 cells (all p < 0.001) but not associated with blood routine (RBC, WBC count, etc.) and liver and renal function indicators (all p > 0.05). By contrast, STAT3 was upregulated. Furthermore, the expression of miR-124 was inversely proportional to that of STAT3 mRNA or protein (p = 0.013, p = 0.015, respectively). In vitro studies demonstrated that the overexpression of miR-124 played a suppressor role in the proliferation of U87 and U251 cells and promoted cell apoptosis. Luciferase reporter assays confirmed that miR-124 binding to the 3'-UTR regions of STAT3 inhibited the expression of STAT3 in U87 and U251 cells. However, the inhibitor of miR-124 promoted the expression of STAT3 and cell proliferation. In conclusion, our data suggest that miR-124 may have a potential role in treatment of GBM patients and that miR-124 is a novel regulator of invasiveness and tumorigenicity in GBM cells by targeting STAT3. The miR-124/STAT3 pathway may be a useful therapeutic agent in GBM patients.

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