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Objective <p>To investigate the role of centrin-2 (CETN2) in platinum resistance and its underlying mechanisms in ovarian cancer.</p> Methods <p>We conducted a pan-cancer analysis of CETN2 expression and its associated genes using the STRING and TIMER databases. Data from the GEO and TCGA databases were employed for survival, clinical correlation, and prognostic analyses. Enrichment and co-expression analyses were performed to identify relevant pathways and genes. We also analyzed the tumor microenvironment, immune checkpoints, and drug sensitivity. For clinical validation, quantitative real-time PCR was used to measure CETN2 expression in patient samples and assess its correlation with chemotherapy response. Predictive models, including logistic regression and decision trees, were constructed. Their performance in predicting chemotherapy outcomes was evaluated using receiver operating characteristic (ROC) curves, and the prognostic impact of CETN2 was assessed via Kaplan-Meier survival analysis.</p> Results <p>CETN2 mRNA expression was significantly elevated in cisplatin-resistant samples. CETN2 was associated with the nucleotide excision repair (NER), oxidative phosphorylation, and cell cycle pathways and showed a negative correlation with several immune checkpoints. CETN2 expression demonstrated notable predictive value for chemotherapy response, particularly in platinum-sensitive ovarian cancer. It influenced stromal and immune-related scores in the tumor microenvironment, and differential expression levels correlated with significant variations in sensitivity to specific drugs. In clinical samples, CETN2 expression was linked to immune infiltration patterns. Protein expression of CETN2 was significantly higher in platinum-resistant patients compared to platinum-sensitive patients and showed predictive utility for chemotherapy outcomes.</p> Conclusion <p>Upregulation of CETN2 may contribute to cisplatin resistance through pathways involving nucleotide excision repair, oxidative phosphorylation, and the cell cycle. CETN2 holds potential as a biomarker for platinum-based chemotherapy response and prognostic evaluation in ovarian cancer.</p>

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Bioinformatics and clinical analysis of CETN2’s impact on platinum resistance and prognosis in epithelial ovarian cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月25日

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  • Lin-yuan Wei,
  • Li Li

摘要

Objective

To investigate the role of centrin-2 (CETN2) in platinum resistance and its underlying mechanisms in ovarian cancer.

Methods

We conducted a pan-cancer analysis of CETN2 expression and its associated genes using the STRING and TIMER databases. Data from the GEO and TCGA databases were employed for survival, clinical correlation, and prognostic analyses. Enrichment and co-expression analyses were performed to identify relevant pathways and genes. We also analyzed the tumor microenvironment, immune checkpoints, and drug sensitivity. For clinical validation, quantitative real-time PCR was used to measure CETN2 expression in patient samples and assess its correlation with chemotherapy response. Predictive models, including logistic regression and decision trees, were constructed. Their performance in predicting chemotherapy outcomes was evaluated using receiver operating characteristic (ROC) curves, and the prognostic impact of CETN2 was assessed via Kaplan-Meier survival analysis.

Results

CETN2 mRNA expression was significantly elevated in cisplatin-resistant samples. CETN2 was associated with the nucleotide excision repair (NER), oxidative phosphorylation, and cell cycle pathways and showed a negative correlation with several immune checkpoints. CETN2 expression demonstrated notable predictive value for chemotherapy response, particularly in platinum-sensitive ovarian cancer. It influenced stromal and immune-related scores in the tumor microenvironment, and differential expression levels correlated with significant variations in sensitivity to specific drugs. In clinical samples, CETN2 expression was linked to immune infiltration patterns. Protein expression of CETN2 was significantly higher in platinum-resistant patients compared to platinum-sensitive patients and showed predictive utility for chemotherapy outcomes.

Conclusion

Upregulation of CETN2 may contribute to cisplatin resistance through pathways involving nucleotide excision repair, oxidative phosphorylation, and the cell cycle. CETN2 holds potential as a biomarker for platinum-based chemotherapy response and prognostic evaluation in ovarian cancer.