Abstract
Diosmetin (Dios), a flavone aglycone, is a major active ingredient of many herbal medicines. Previous studies implicated that the potential antitumor activities of Dios are mediated through multiple cell signaling pathways, however more investigations are required to reveal the targets and mechanisms of Dios. In this study, our results demonstrated that cell cycle progression and proliferation of HepG2 cells were inhibited by Dios. Meanwhile, Dios-induced liver cancer cell apoptosis was related with the p53 activation. After PFT-α, a p53 inhibitor was added into Dios-treated HepG2 cells, cell growth inhibition was partially reversed. These findings defined and supported that p53 is a novel target of Dios. By activating p53, Dios exerts anticancer effects by inducing cell cycle arrest and apoptosis in HepG2 cells.
Keywords: Diosmetin, HepG2, P53, apoptosis, flavonoids, ERK and JNK phosphorylation.
Graphical Abstract