Abstract
Background Endometrial cancer (EC) is a common tumor of the genital tract that affects the female reproductive system but with only limited treatment options. We aimed to discover new prognostic biomarkers for EC. Methods We used mRNA-seq data to detect differentially expressed genes (DEGs) between EC and control tissues. Detailed clinicopathological information was collected, and changes in the mRNA and protein levels of hub DEGs were analyzed in EC. Copy number variation (CNV) was also evaluated for its association with the pathogenesis of EC. Gene set enrichment analysis (GSEA) was conducted to enrich significant pathways driven by the hub genes. Cox regression analysis was used to select variables to create a nomogram. The nomogram was calibrated by applying the concordance index (C-index), and net benefits of the nomogram at different threshold probabilities were quantified using decision curve analysis (DCA). Results Differential expression analysis identified 24 DEGs as potential risk factors for EC. Survival analysis revealed that TPX2 expression was related to worsening overall survival in patients with advanced EC. A high CNV was associated with the overexpression of TPX2; this suggested that modifications in the cell-cycle pathway might be crucial in the advancement of EC. Moreover, an individualized nomogram was developed for TPX2 incorporating clinical factors; this was also evaluated for its ability to predict EC. Calibration and DCA analyses confirmed the robustness and clinical usefulness of the nomogram. Conclusion We offer novel insights into the pathogenesis and molecular mechanisms of EC. The overexpression of TPX2 was related to a poorer prognosis and could serve as a biomarker for predicting prognostic outcomes in EC patients.
Highlights
Endometrial cancer (EC) is the sixth most frequent malignancy among women worldwide [1]
In the TCGA Uterine Corpus Endometrial Carcinoma (UCEC) dataset, we identified 1087 upregulated genes and 411 downregulated genes (Figure 2(c))
We revealed a correlation between targeting protein for Xenopus kinesin-like protein 2 (TPX2) overexpression and copy number amplification in EC patients, especially those with Federation Internationale de Gynecologie et d’Obstetrique (FIGO) stages III and IV; these stages are strongly associated with a poor prognosis. ese data indicate that TPX2 copy number gains may play a key role in carcinogenesis and disease progression
Summary
Endometrial cancer (EC) is the sixth most frequent malignancy among women worldwide [1]. The survival rates of patients in the advanced stages range from 20% to 40% [2]. Similar to other proteins that regulate mitosis, TPX2 is overexpressed in a range of different cancers and is generally associated with a poor. Differential expression analysis identified 24 DEGs as potential risk factors for EC. Survival analysis revealed that TPX2 expression was related to worsening overall survival in patients with advanced EC. A high CNV was associated with the overexpression of TPX2; this suggested that modifications in the cell-cycle pathway might be crucial in the advancement of EC. An individualized nomogram was developed for TPX2 incorporating clinical factors; this was evaluated for its ability to predict EC. E overexpression of TPX2 was related to a poorer prognosis and could serve as a biomarker for predicting prognostic outcomes in EC patients We offer novel insights into the pathogenesis and molecular mechanisms of EC. e overexpression of TPX2 was related to a poorer prognosis and could serve as a biomarker for predicting prognostic outcomes in EC patients
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