ArticleDiscover oncology2025
Targeting NADPH oxidase 2 suppresses the growth of esophageal squamous cell carcinoma by regulating BTG2 pathway.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNicotinamide 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
methodsNOX2 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.
resultsNOX2 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.
conclusionThe 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.
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