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Background <p>Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) plays a carcinogenic role in various tumors. Recent study has reported that the carcinogenic mechanism of NOX2 in esophageal squamous cell carcinoma (ESCC) may be associated with the regulation of B-cell translocation gene 2 (BTG2). This study aims to clarify the role of NOX2 in the progression of ESCC.</p> Materials and methods <p>NOX2 was knocked down in ESCC cell lines via siRNA transfection to assess its impact on cell function and BTG2 regulation. Tumor tissues from 66 ESCC patients were analyzed for NOX2 and BTG2 expression using immunohistochemistry to determine their clinical significance.</p> Results <p>NOX2 deficiency inhibited ESCC cell proliferation, promoted apoptosis, and caused G1 phase arrest. Following NOX2 knockdown, BTG2 mRNA expression significantly increased in TE1 and KYSE30 cells, and a notable rise in BTG2 protein expression was observed in KYSE30 cells. Immunohistochemical analysis revealed that NOX2 expression was significantly higher in tumor tissues compared to adjacent non-cancerous tissues, while BTG2 expression was markedly lower in tumor tissues. High NOX2 expression correlated with poor prognosis, whereas high BTG2 expression indicated better outcomes. Multivariate analysis indicated that abnormal NOX2 and BTG2 expressions are independent prognostic factors for ESCC.</p> Conclusion <p>The carcinogenic role of NOX2 in ESCC may be associated with the regulation of BTG2 expression. The aberrant expressions of NOX2 and BTG2 are associated with the prognosis of patients with ESCC, suggesting that NOX2 and BTG2 could serve as potential biomarkers and therapeutic targets.</p>

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Targeting NADPH oxidase 2 suppresses the growth of esophageal squamous cell carcinoma by regulating BTG2 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Xiao-Jie Liu,
  • Can-Lin Yang,
  • Yun-Lei Zhang,
  • Jun-Xing Huang

摘要

Background

Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) plays a carcinogenic role in various tumors. Recent study has reported that the carcinogenic mechanism of NOX2 in esophageal squamous cell carcinoma (ESCC) may be associated with the regulation of B-cell translocation gene 2 (BTG2). This study aims to clarify the role of NOX2 in the progression of ESCC.

Materials and methods

NOX2 was knocked down in ESCC cell lines via siRNA transfection to assess its impact on cell function and BTG2 regulation. Tumor tissues from 66 ESCC patients were analyzed for NOX2 and BTG2 expression using immunohistochemistry to determine their clinical significance.

Results

NOX2 deficiency inhibited ESCC cell proliferation, promoted apoptosis, and caused G1 phase arrest. Following NOX2 knockdown, BTG2 mRNA expression significantly increased in TE1 and KYSE30 cells, and a notable rise in BTG2 protein expression was observed in KYSE30 cells. Immunohistochemical analysis revealed that NOX2 expression was significantly higher in tumor tissues compared to adjacent non-cancerous tissues, while BTG2 expression was markedly lower in tumor tissues. High NOX2 expression correlated with poor prognosis, whereas high BTG2 expression indicated better outcomes. Multivariate analysis indicated that abnormal NOX2 and BTG2 expressions are independent prognostic factors for ESCC.

Conclusion

The carcinogenic role of NOX2 in ESCC may be associated with the regulation of BTG2 expression. The aberrant expressions of NOX2 and BTG2 are associated with the prognosis of patients with ESCC, suggesting that NOX2 and BTG2 could serve as potential biomarkers and therapeutic targets.