ObjectiveThis study aims to explore the role of CBLL1 in pan-carcinoma and tumor immune infiltrates. MethodsDownload mRNA expression, mutation and clinical data in UCSC database, to analyze the relationship between CBLL1 expression and clinicopathological vlaue, and immune microenvironment in pan-cancer. CIBERSORT was used to analyze the relationship between CBLL1 expression and the infiltration of pan-carcinoma immune cells. The mRNA expression data of UCSC database were used to analyze the correlation between CBLL1 expression and pan-cancer immunomodulations, checkpoints and receptor molecules. ResultsThe levels of CBLL1 mRNA expression in pan-cancer tissues were abnormal. The level of CBLL1 is related to the age, race, clinical stage and treatment effect of patients with pan-carcinoma and associated with the prognosis of patients with KIRC, LUSC, THCA, THYM, MESO, PRAD, STAD, and UVM. Univariate COX regression analysis showed that expression of CBLL1 was a risk factor for poor prognosis in patients with KICH, KIRC, LAML, THYM, KIRC, PCPG, OV, PRAD, STAD, GBM and UVM. The expression level of CBLL1 was correlated with BLCA, BRCA, COAD, LAML, LGG, LUAD, LUSC, SARC, STAD, THCA, THYM and UVM tumor mutational burden, and with ACC, BRCA, CESC, COAD, DLBC, HNSC, PRAD, READ, SARC, STAD, TGCT, THCA and UCEC microsatellite instability. The expression level of CBLL1 was correlated with cancer stromal cells and immune cells. The expression of CBLL1 is related to pan-cancer immunomodulators, checkpoints and receptor molecules. ConclusionCBLL1 is abnormally expressed in patients with pan-carcinoma, which is expected to be a biomarker for prognosis, mutation and immune infiltration in patients with pan-carcinoma.
Background: Esophageal cancer is one of the most common malignant tumors. The purpose of this study was to reveal the expression of LGALS1 in esophagus cancer (ESCA) and its clinical value, and to explore the mechanism of LGALS1 in the occurrence and development of ESCA.Methods: Oncomine, Tumor Immune Estimation Resource (Timer) and The Cancer Genome Atlas (TCGA) database were used to analyze the expression of LGALS1 in ESCA and its value in the diagnosis of ESCA. The correlation between LGALS1 and the clinicopathological characteristics of ESCA patients was analyzed in the Ualcan database. In TCGA database, we performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) to elucidate the potential mechanism underlying the role of LGALS1 in ESAC. LGALS1 co-expressed genes were imported into the String database to build a protein-protein interaction (PPI) network. The CytoHubba plug-in in Cytoscape was used to screen the hub gene and was verified in Gene Expression Profiling Interactive Analysis (GEPIA) and TCGA database.Results: LGALS1 was highly expressed in ESCA tissues. Increasing the expression level of LGALS1 was related to age, ethnicity, clinical stage, tumor grade, and histological subtype of ESCA patients, and receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) was 0.8511 (P <0.001). There are 482 LGALS1 co-expressed genes. GO and KEGG show that LGALS1 co-expressed genes are mainly involved in endothelial cell differentiation, transforming growth factor receptor signaling pathway, epithelial cell proliferation, ECM receptor interactions, leukocyte migration, transcriptional disorders during cancer, PI3K/AKT signaling pathway and other processes. GSEA showed that elevated LGALS1 was mainly enriched for ECM receptor interactions, cancer pathways, and TGF BETA signaling pathways. The Hub genes COL1A1, FN1, COL1A2, COL3A1, COL5A1, COL5A2, COL4A2, COL18A1, and COL6A1 are higher expressed in ESCA tissues and have diagnostic significance in ESCA.Conclusion: LGALS1 expression is elevated in ESCA patients and may be a potential diagnostic marker for ESCA patients. PI3K/AKT signaling pathway, TGF BETA signaling pathway, cancer pathway, cytokine and cytokine interaction may be an important pathway for regulation in occurrence and development of ESCA.
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