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<p>Oral submucous fibrosis (OSF) is a precancerous oral condition, with betel quid chewing and smoking identified as potential risk factors. However, the relationship between these factors, particularly their interaction, remains inconclusive. In this study, we observed that low-dose nicotine exposure (&lt; 500&#xa0;nM) increased arecoline-induced proliferation of human oral mucosa fibroblasts, whereas high doses of nicotine (1000&#xa0;nM and 5000&#xa0;nM) inhibited fibroblast proliferation. Our experiments elucidated the essential role of the Egr-1/Wnt5a pathway in nicotine-induced fibroblast proliferation. Nicotine amplified the impact of arecoline by further activating the Egr-1/Wnt5a pathway. Upon exposure to nicotine (250&#xa0;nM) with or without arecoline, the expression of Egr-1 mRNA remained unaltered, yet Egr-1 and Wnt5a protein levels increased. Interestingly, Egr-1 exhibited enhanced stability in nicotine-treated cells, regardless of the presence of arecoline. Thus, it is evident that low-dose nicotine promotes arecoline-induced proliferation of human oral mucosa fibroblasts by enhancing the stability of the Egr-1 protein.</p> Graphical Abstract <p></p>

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Low-dose nicotine enhances arecoline-induced human oral mucosa fibroblast proliferation by stabilizing Egr-1 protein

  • 期刊论文

  • 发表日期：

    2025年8月18日

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  • Qiang Chen,
  • Shuiping Liu,
  • Yun Zhang,
  • Da Zheng,
  • Qianqian Ma,
  • Jianrui Wei,
  • Xiaoshan Liu,
  • Dandan Hu,
  • Bo Xie

摘要

Oral submucous fibrosis (OSF) is a precancerous oral condition, with betel quid chewing and smoking identified as potential risk factors. However, the relationship between these factors, particularly their interaction, remains inconclusive. In this study, we observed that low-dose nicotine exposure (< 500 nM) increased arecoline-induced proliferation of human oral mucosa fibroblasts, whereas high doses of nicotine (1000 nM and 5000 nM) inhibited fibroblast proliferation. Our experiments elucidated the essential role of the Egr-1/Wnt5a pathway in nicotine-induced fibroblast proliferation. Nicotine amplified the impact of arecoline by further activating the Egr-1/Wnt5a pathway. Upon exposure to nicotine (250 nM) with or without arecoline, the expression of Egr-1 mRNA remained unaltered, yet Egr-1 and Wnt5a protein levels increased. Interestingly, Egr-1 exhibited enhanced stability in nicotine-treated cells, regardless of the presence of arecoline. Thus, it is evident that low-dose nicotine promotes arecoline-induced proliferation of human oral mucosa fibroblasts by enhancing the stability of the Egr-1 protein.

Graphical Abstract