Roles Of Med27 In Regulating Glioma Cells Via Nf-Kappa B Inos

Neuroglioma is one major challenge in neurosurgery, due to its complicated pathogenesis mechanism, which has not been fully resolved yet. The identification of effective molecular targets for pathogenesis of neuroglioma thus can benefit the treatment efficacy of glioma. Previous study found that mediator complex 27 (MED27) was involved in mediating tumor occurrence and progression. The role of MED27 in glioma and related mechanism, however, has not been illustrated. In vitro cultured glioma U87 cells were randomly divided into control group, scramble group, which received negative controlled siRNA, and MED27 siRNA transfection group. Real-time PCR was used to detect the expression of MED27 mRNA, while Western blotting was used for analyzing MED27 protein. MTT assay and invasion assay were used to detect the effect of MED27 on U87 cell proliferation and invasion. Caspase-3 activity assay was used to reveal U87 apoptosis, followed by Western blotting to detect NF-kappa B/iNOS protein expression. After transfecting MED27 siRNA, expression of MED27 protein was decreased, leading to inhibition of U87 cell proliferation or invasion, in addition to enhanced caspase3 activity (p < 0.05 compared to control group). The transfection of MED27 siRNA significantly down-regulated the expression of NF-kappa B/iNOS protein in glioma cells (p < 0.05 compared to control group). The inhibition of MED27 facilitates glioma cell apoptosis, inhibits their proliferation or invasion, mainly via suppressing NF-kappa B/iNOS signal pathway.