Inhibition of TP53 Mutant Oral Cancer by Reactivating p53

Background: Mutation of p53 is a frequent event, and mutant exhibits low levels acetylation phosphorylation. This study aimed to investigate the effect histone deacetylase (HDAC) inhibitor, 4-hexylresorcinol (4HR), on phosphorylation carcinoma cells its therapeutic effects in xenograft model. Methods: To determine 4HR p53, western blot analysis was performed using YD-9 YD-15 cells. siRNA used examine whether acts p53-dependent or independent manner. evaluated Results: In vitro experiments when concentration increased, expression HDAC4, acetylated (Ac-p53), phosphorylated (p-p53) increased. Transfection with TP53 successfully suppressed protein mRNA expression. When administered model, tumour expansion rate compared control, mice exhibited higher survival rate. Conclusions: Our findings reveal that potential agent restores loss function cancer via as well inhibition HDAC4.