Glioblastoma is one of the leading cancer-related causes of death of the brain region and has an average 5-year survival rate of less than 5%. The aim of this study was to investigate the effectiveness of tectorigenin, a naturally occurring flavonoid compound with anti-inflammatory, anti-oxidant, and anti-tumor properties, as a treatment for glioblastoma. A further goal was to use in vitro models to determine the underlying molecular mechanisms. Exposure to tectorigenin for 24 h dose-dependently reduced the viability of glioblastoma cells. Significant cell cycle arrest at G0/G1 phase occurred in the presence of 200 and 300 µM tectorigenin. Treatment with tectorigenin clearly reduced the levels of phosphorylated retinoblastoma protein (p-RB) and decreased the expression of cyclin-dependent protein 4 (CDK4). Tectorigenin treatment also significantly enhanced the expression of p21, a CDK4 inhibitor. Collectively, our findings indicated that tectorigenin inhibited the proliferation of glioblastoma cells by cell cycle arrest at the G0/G1 phase.
Keywords: cell cycle arrest; glioblastoma; in vitro model; molecular mechanism; tectorigenin.