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Background <p>Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral and maxillofacial regions. Paeonol, derived from <i>Moutan Cortex</i>, has diverse pharmacological effects including anti-inflammatory and anticancer activities. The N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac<sup>4</sup>C) modification is a newly discovered RNA epigenetic mechanism. This study aimed to investigate the role of paeonol in OSCC and its underlying mechanisms of action.</p> Methods <p>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.</p> Results <p>The results showed that paeonol treatment decreased the viability, migration, and glycolysis of OSCC cells. Moreover, paeonol treatment inhibited NAT10-mediated ac<sup>4</sup>C modifications in OSCC cells. In addition, NAT10 overexpression upregulates glycolysis and cell migration in OSCC cells. Moreover, NAT10 upregulated ac<sup>4</sup>C levels of HK2 in OSCC cells. Animal studies have revealed that paeonol treatment decreases OSCC tumor growth.</p> Conclusion <p>This study revealed that paeonol inhibited glycolysis and cell migration in OSCC by suppressing the NAT10-mediated ac<sup>4</sup>C modification of HK2.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月7日

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  • Kang Yang,
  • Baosen Yue,
  • Huan Tian,
  • Lu Wang,
  • Xiao Yang,
  • Weiying Zhang

摘要

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 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, 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.