Scutellarin inhibits glioma cell proliferation by up-regulating miR-15a expression

Objective: To investigate the effect of scutellarin on the proliferation of glioma cells through microRNA (miR)-15a. Methods: Human glioma cell line T98G was cultured in vitro and divided into control group (without treat-ment), scutellarin group (with 10, 20, 40, 80, 160 pg/mL scutellarin, respectively), miR-15a negative control group (transfected with negative control-miR-15a + 80 pg/mL scutellarin) and miR-15a inhibitor group (transfected with miR-15a siRNA + 80 pg/mL scutellarin). The proliferation of T98G cells was detected by cell counting kit-8 (CCK-8), and the expression of miR-15a in T98G cells was detected by real-time fluorescence quantitative PCR (qRT-PCR). The apoptosis of T98G cells was assessed by flow cytometry, and the invasion of T98G cells was compared by Transwell method. The levels of proliferating cell nuclear antigen (PCNA), Bcl-2 related X protein (Bax) and matrix metalloproteinase 9 (MMP-9) in T98G cells were detected by Western blot (WB). Results: Compared with that in the control group, the OD value of T98G cells in scutellarin group was significantly lower (P<0.05), with the increase of scutellarin concentration, the OD value of T98G cells decreased in turn, and 80 pg/mL was used as the optimal concentration of scutellarin to treat T98G cells for subsequent experiments. Compared with those in the control group, the miR-15a expression, apoptosis rate and Bax protein expression in T98G cells of scutellarin group were higher (P<0.05), and the OD value, number of invasive cells, PCNA and MMP-9 protein levels were lower (P<0.05). Compared with scutellarin group and miR-15a negative control group, the miR-15a expression, apoptosis rate and Bax protein expression in T98G cells of miR-15a inhibitor group were lower (P<0.05), and the OD value, number of invasive cells, PCNA and MMP-9 protein levels were higher (P<0.05). Conclusions: Scutellarin can inhibit the prolif-eration, invasion and induce the apoptosis of glioma cells, which may be mediated by up-regulating the expression of miR-15a.