AIM: To investigate the regulation of miR-21 on FasL expression and its effect on the growth and apoptosis in glioma cells, and to evaluate the molecular mechanism. METHODS: Differential expression levels of miR-21 in human glioma U251 cells were achieved by transfecting with miR-21 mimics, miR-21 inhibitor or scramble. The viability and apoptosis of U251 cells were detected by CCK-8 assay and flow cytometry with Annexin V- FITC/PI double staining. The recombination vector pmirGLO-FasL was constructed. Dual-luciferase reporter experiment was performed to validate the target genes of miR-21. The expression vector pcDNA3.1-FasL was also constructed, and the biological activity and regulatory role of miR-21 in U251 cell apoptosis were analyzed by a restore experiment. RESULTS: Exogenous overexpression of miR-21 increased the viability and decreased the apoptosis of U251 cells (P<0.05), while miR-21 inhibitors generated the opposite results (P<0.05). Dual-luciferase reporter assay and restore experiment revealed that miR-21 negatively regulated the expression of FasL gene which was regarded as the target gene, thus decreasing the apoptosis of U251 cells. CONCLUSION: miR-21 increases the viability of glioma U251 cells, in which FasL may be one of the target genes.
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