Molecular mechanisms by which C1orf112 promotes endometrial cancer progression and the development and validation of...

To investigate the expression profile, clinical significance, and underlying molecular mechanisms of C1orf112 in endometrial cancer (EC).

We performed bioinformatics analyses using data from The Cancer Genome Atlas to evaluate C1orf112 expression and its association with clinicopathological parameters in EC. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, as well as protein-protein interaction network analysis, were conducted to explore the functional roles and regulatory pathways of C1orf112. A multi-omics integrative approach was used to elucidate the regulatory mechanisms underlying C1orf112 expression. Furthermore, we constructed and validated a prognostic scoring model incorporating C1orf112 expression.

C1orf112 was found to be significantly highexpressed in EC tissues and its expression was closely associated with clinical stage, histological grade, and patient prognosis. Functional enrichment analyses indicated that C1orf112 and its co-expressed genes are primarily involved in cell cycle regulation, DNA replication, and the p53 signaling pathway. Notably, our bioinformatics predictions suggest that C1orf112 may be subject to bidirectional regulation by RNA-binding proteins, including LIN28B and SRRM4, potentially establishing a regulatory balance between oncogenic and tumor-suppressive pathways. Multi-omics analysis demonstrated that C1orf112 expression is co-regulated by genetic alterations and epigenetic modifications, with promoter DNA methylation levels showing a strong inverse correlation with transcriptional activity. However, further molecular and phenotypic validation is required to confirm these interactions. The prognostic scoring model incorporating C1orf112 expression exhibited robust predictive performance.

Our findings highlight the potential clinical utility of C1orf112 as a diagnostic and prognostic biomarker in EC, and provide new insights into its regulatory molecular network. This study proposes a conceptual framework for understanding EC pathogenesis and guiding the development of targeted therapies. Nonetheless, further prospective clinical studies and mechanistic investigations are warranted to validate these findings.