In-Silico Multi-Omics Analysis of the Functional Significance of Calmodulin 1 in Multiple Cancers
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Aberrant activation of calmodulin 1 () has been reported in human cancers. However, comprehensive understanding of the role of in most cancer types has remained unclear. We systematically analyzed the expression landscape, DNA methylation, gene alteration, immune infiltration, clinical relevance, and molecular pathway of in multiple cancers using various online tools, including The Cancer Genome Atlas, cBioPortal and the Human Protein Atlas databases. Kaplan-Meier and receiver operating characteristic (ROC) curves were plotted to explore the prognostic and diagnostic potential of expression. Multivariate analyses were used to evaluate whether the expression could be an independent risk factor. A nomogram predicting the overall survival (OS) of patients was developed, evaluated, and compared with the traditional Tumor-Node-Metastasis (TNM) model using decision curve analysis. R language was employed as the main tool for analysis and visualization. Results revealed to be highly expressed in most cancers, its expression being regulated by DNA methylation in multiple cancers. had a low mutation frequency (within 3%) and was associated with immune infiltration. We observed a substantial positive correlation between expression and macrophage and neutrophil infiltration levels in multiple cancers. Different mutational forms of hampered immune cell infiltration. Additionally, expression had high diagnostic and prognostic potential. Multivariate analyses revealed expression to be an independent risk factor for OS. Therefore, our newly developed nomogram had a higher clinical value than the TNM model. The concordance index, calibration curve, and time-dependent ROC curves of the nomogram exhibited excellent performance in terms of predicting the survival rate of patients. Moreover, elevated expression contributes to the activation of cancer-related pathways, such as the and pathways. Overall, our findings improved our understanding of the function of in human cancers.
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