Paeonol inhibits the Glycolysis in oral squamous cell carcinoma though suppressing NAT10-mediated ac4C modification

Paeonol inhibits the Glycolysis in oral squamous cell carcinoma though suppressing NAT10-mediated ac4C modification

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Abstract Background Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral and maxillofacial regions.Paeonol, derived from Moutan Cortex, has diverse pharmacological effects including anti-inflammatory and anticancer activities.The N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification is a newly discovered RNA epigenetic mechanism.

This 2000 bmw 528i front bumper study aimed to investigate the role of paeonol in OSCC and its underlying mechanisms of action.Methods Cell viability and migration were assessed using a cell counting kit-8 and transwell migration assays.Glycolysis-related indices were detected using commercial kits.

The interaction between NAT10 and hexokinase 2 (HK2) was examined using RNA immunoprecipitation and dual-luciferase reporter assays.A tumor-bearing mouse model was established.Results The results showed that paeonol treatment decreased the viability, migration, and glycolysis of OSCC cells.

Moreover, paeonol treatment inhibited NAT10-mediated ac4C modifications in OSCC cells.In addition, NAT10 overexpression upregulates glycolysis and cell migration in OSCC cells.Moreover, 15-eg1053cl NAT10 upregulated ac4C levels of HK2 in OSCC cells.

Animal studies have revealed that paeonol treatment decreases OSCC tumor growth.Conclusion This study revealed that paeonol inhibited glycolysis and cell migration in OSCC by suppressing the NAT10-mediated ac4C modification of HK2.