The global burden of
malignant glioma is expected to increase and new
therapy approaches are urgently required.
Solasonine is a natural glycoalkaloid compound that has been used in
cancer treatment for many years; however the precise mechanisms are poorly understood. Here we seek to explore the potential roles of
solasonine in
glioma that could add to the development of newer therapeutic approaches for the treatment of
malignant glioma. Cell proliferation of
glioma cells was determined by MTT assay, and the biological functions of
solasonine were investigated by migration, colony formation, apoptosis assays and cell cycle analysis in
glioma cells. Western blotting and RT-qPCR were used to detect the
protein and gene expression levels respectively. The nuclear localization of NF-κB p50/p65 was analyzed
after treatment with
solasonine. The roles of MAPKs in the anticancer effect of
solasonine were then examined. The in vivo anti-
tumor efficacy of
dopamine was also analyzed in xenografts nude mice. We report that
solasonine could inhibit cell proliferation, migration and colony formation of
glioma cells. Treatment of
solasonine induced apoptosis via modulating
cytochrome c and
caspase signaling. Besides,
solasonine decreased the expression of proinflammatory mediators and nuclear translocalization of NF-κB p50/p65. Mechanistic investigation further revealed that
solasonine may target anti-inflammatory signaling pathway, and more specifically p-p38 and p-JNK MAPKs. All these indicated that
solasonine could inhibit
glioma growth via inhibiting inflammatory signaling pathway.