Magnolol induces human Ewing sarcoma SK-ES-1 cell apoptosis via the mitochondrial and death receptor pathways.

New treatments for Ewing's sarcoma (ES) are urgently needed. Magnolol, an active ingredient in Magnolia officinalis, shows anti-oxidative, anti-microbial, and anti-tumor effects, but its effect on ES is unknown. We examined the effect of magnolol on ES cell proliferation and apoptosis in vitro as well as the mechanism of its anticancer effect. The results demonstrated that magnolol inhibited the proliferation of ES and induced ES cell apoptosis through the mitochondrial and death receptor pathways. Magnolol reduced MEK1/2, ERK1/2, and STAT3 phosphorylation in ES cells, suggesting that the MAPK/ERK and JAK/STAT3 signal transduction pathways are involved in the inhibition of ES cell growth by magnolol. In short, magnolol is a potential anti-ES drug.