Abstract
Neuroglioma is the most common primary malignant tumor in neurosurgery. Due to its short survival period and high patient mortality rate, neuroglioma is a major challenge in clinics. Elucidating the pathogenic mechanisms and associated molecular targets of neuroglioma can therefore benefit diagnosis and treatment of glioma. Previous studies have established the role of microRNA (miR)‑26b in various tumors, including breast cancer, lymphoma and glioma. Its function and mechanism in neuroglioma, however, remains to be elucidated. In the present study, in vitro cultured U87 glioma cells were randomly divided into miR‑26b mimic, miR‑26b inhibitor and respective control (NC) groups. MTT assay was performed to detect the effect of miR‑26b on cell proliferation, while a cell invasion assay detected its effects on cell invasion. Caspase‑3 activity was also quantified to test cell apoptosis, followed by reverse transcription-quantitative polymerase chain reaction and western blotting to detect the variation of Bcl‑2 expression under the effect of miR‑26b. miR‑26b mimics transfection upregulated its expression in U87 cells, which had significantly reduced Bcl‑2 mRNA and protein expression levels and higher casapse3 activity, and inhibited cell proliferation and invasion compared with the control group. The transfection of miR‑26b inhibitor, in contrast, facilitated U87 cell proliferation and invasion, inhibited caspase‑3 activity and elevated Bcl‑2 mRNA/protein expression. In conclusion, miR‑26 could facilitate apoptosis and inhibit proliferation/invasion of neuroglioma cells via downregulating Bcl‑2 expression and potentiating caspase-3 activity.