Effects of norcantharidin on proliferation and apoptosis of glioma cells via mitogen-activated protein kinase/extracellular regulated protein kinase signaling pathway

Abstract

Objective To investigate the effects of norcantharidin (NCTD) on the proliferation and apoptosis on glioma cells. Methods Glioma U87 cells were treated with various concentrations of NCTD (25, 50, 100, 200 μmol/L) for 24, 48 h. The effects of NCTD on the proliferation and apoptosis of glioma cells were measured by methyl thiazol tetrazolium (MTT) assay and flow cytometry. The Mitogen-activated protein kinase/extracellular regulated protein kinase (MAPK/ERK) signaling pathway changes were detected by Western blotting. Results The results showed that NCTD effectively inhibited cell growth and induced apoptosis in U87 cells in a time- and dose-dependent manner. After incubation with NCTD for 24 h and 48 h, the average half maximal inhibitory concentration (IC50) was 147.7 μmol/L and 62.5 μmol/L, respectively. It could significantly inhibit proliferation at 24 h and 48 h (F=30.234, 42.106, P=0.000). As compared with the control group [(1.2±0.9)%], the cell apoptosis rate induced by 30, 50 μmol/L of NCTD for 10 h was (6.8±1.2)% and (17.2±2.0)%, respectively, which indicated that NCTD could induce apoptosis of cells in a dose-dependent manner (F=405.761, P=0.000). Western blotting results revealed that the phospho-MEK and phospho-ERK were down-regulated significantly in NCTD group as compared with control group (P=0.007). Conclusion Our findings demonstrated that NCTD inhibited proliferation and induced apoptosis of U87 glioma cells through MAPK/ERK signaling pathway. Key words: Glioma; Norcantharidin; Mitogen-activated protein kinase/extracellular regulated protein kinase signaling pathway; Apoptosis