<i>CLIP2</i> is a potential biomarker for platinum resistance and prognosis in ovarian cancer: a bioinformatics analysis

<h4>Background</h4>Ovarian cancer exhibits the highest mortality rate among gynecologic malignancies. Platinum resistance remains a key determinant of poor clinical outcomes. Early prediction of platinum resistance is critical for personalized treatment. This study aimed to identify <i>CLIP2</i> as an independent prognostic biomarker and assess its predictive value for platinum resistance and the tumor immune microenvironment in ovarian cancer.<h4>Methods</h4>Through integrated bioinformatics analysis of ovarian cancer cohorts from TCGA and GEO, we performed differential gene expression profiling, survival analysis, and multivariate Cox regression to identify biomarkers associated with platinum resistance and prognosis. A <i>CLIP2</i>-based logistic regression model was constructed and evaluated using leave-one-out cross-validation (LOOCV). TCGA patients were stratified by <i>CLIP2</i> expression for comparative analyses of overall survival, mutational landscapes, drug sensitivity, and immunogenomic characteristics.<h4>Results</h4><i>CLIP2</i> was identified as an independent predictor of platinum resistance and a significant prognostic biomarker (HR = 1.20; 95% CI: 1.05-1.40; p = 0.007). The <i>CLIP2</i>-based model achieved an AUC of 0.68. The high-<i>CLIP2</i> subgroup exhibited significantly poorer overall survival (log-rank p = 0.04) and distinct somatic mutation profiles. Drug sensitivity analysis revealed that high <i>CLIP2</i> expression conferred resistance to platinum-based agents, topotecan, and gemcitabine, but heightened sensitivity to olaparib, cediranib, and pictilisib. Immunogenomic profiling further indicated that <i>CLIP2</i> overexpression was associated with an immunosuppressive microenvironment, characterized by depleted infiltration of activated dendritic cells, CD8⁺ T cells, M1 macrophages, and helper T cells, alongside positive correlations with inhibitory checkpoints (<i>CD276</i>, <i>ADORA2A</i>, and <i>ENTPD1</i>) and negative correlations with stimulatory checkpoints (<i>CD48</i> and <i>NCR3</i>).<h4>Conclusions</h4>Through bioinformatic analysis, this study proposes <i>CLIP2</i> as a potential biomarker associated with platinum resistance and immune microenvironment patterns in ovarian cancer. These preliminary findings provide a basis for subsequent mechanistic studies and larger validation cohorts to confirm its clinical relevance in guiding immunotherapy and targeted treatment approaches.