Taxifolin Inhibits the Proliferation of Glioblastoma Multiforme Cells via Apoptosis and Autophagy

Abstract

Glioblastoma multiforme is the most malignant tumor in the central nervous system. As a result of its high recurrence rate, drug resistance, and distal metastasis, the 5-year survival rate of glioblastoma multiforme patients is only around 5%. Taxifolin, a polyphenol from traditional Chinese medicine, exerts antioxidant, anti-inflammatory, and antitumor properties. This study aimed to explore the molecular mechanisms of taxifolin on the proliferation of glioblastoma multiforme. Taxifolin mitigated the viability of GBM 8901 cells in a time- and dose-dependent manner. Flow cytometry analysis by PI alone or PI combined with Annexin V revealed that taxifolin at 200 and 400 μM significantly elevated the apoptosis population in GBM8901 cells. Western blot analysis demonstrated that taxifolin dose-dependently increased p53 expression and reduced poly ADP-ribose polymerase, B-cell lymphoma 2, and pro-caspase-3 expression. Moreover, the autophagy-related protein p62 was reduced by taxifolin. By contrast, expression of the light chain 3β protein was elevated in response to taxifolin treatment. Depletion of light chain 3β protein by short hairpin RNA significantly recovered 200 and 400 μM taxifolin-induced cell death in GBM8901 cells. Our findings indicated that taxifolin repressed the cell proliferation of glioblastoma multiforme by triggering apoptosis and autophagy. Using taxifolin to treat glioblastoma multiforme may be a potential therapy agent.