Abstract
BackgroundThe function of collagen triple helix repeat containing 1 (CTHRC1) as an oncogene has been reported in a growing number of publications. Bioinformatics methods represent a beneficial approach to examine the mechanism and function of the CTHRC1 gene in the disease process of cancers from a pan-cancer perspective.MethodsIn this study, using the online databases UCSC, NCBI, HPA, TIMER2, Oncomine, GEPIA, UALCAN, cBioPortal, COSMIC, MEXPRESS, STRING, CCLE, LinkedOmics, GTEx, TCGA, CGGA, and SangerBox, we focused on the relationship between CTHRC1 and tumorigenesis, progression, methylation, immunity, and prognosis. qPCR was used to detect CTHRC1 expression in glioma tissues and cell lines.ResultsThe pan-cancer analysis showed that CTHRC1 was overexpressed in most tumors, and a significant correlation was observed between CTHRC1 expression and the prognosis of patients with cancer. CTHRC1 genetic alterations occur in diverse tumors and are associated with tumor progression. Levels of CTHRC1 promoter methylation were decreased in most cancer tissues compared with normal tissues. In addition, CTHRC1 coordinated the activity of ICP genes through diverse signal transduction pathways, was also associated with immune cell infiltration and the tumor microenvironment, and potentially represented a promising immunotherapy target. We identified CTHRC1-related genes across cancers using the GEPIA2 tool. The single-gene GO analysis of CTHRC1 across cancers showed that it was involved in some signaling pathways and biological processes, such as the Wnt signaling pathway, cell migration, and positive regulation of protein binding. The expression and function of CTHRC1 were also further verified in glioma tissues and cell lines.ConclusionsCTHRC1 is overexpressed in various cancer types and functions as an important oncogene that may promote tumorigenesis and development through different mechanisms. CTHRC1 may represent an important therapeutic target for human cancers.
Highlights
The function of collagen triple helix repeat containing 1 (CTHRC1) as an oncogene has been reported in a growing number of publications
We first performed an analysis of the pattern of CTHRC1 expression in various normal tissues and tumor/nontumor cells
CTHRC1 expression is low in most normal tissues, it is detectable (NX > 1), indicating that the CTHRC1 mRNA has low tissue specificity
Summary
The function of collagen triple helix repeat containing 1 (CTHRC1) as an oncogene has been reported in a growing number of publications. Mediated by the transcriptional coactivator β-catenin, the canonical Wnt pathway serves as one of the essential cellular signaling pathways that contributes to controlling embryogenic developmental processes, tissue homeostasis and carcinogenesis [1]. Various studies indicate that CTHRC1 regulates tumor progression through CTHRC1/Wnt/β-catenin pathways [6,7,8,9,10,11,12]. By inducing the transcription of downstream target genes (such as cyclin D1, CD44, and c-Myc) and promoting β-catenin nuclear translocation, CTHRC1 regulates tumor development [8]. Another study showed that the CTHRC1 promoter region is regulated by β-catenin, inducing CTHRC1 transcription [9]. The interaction network between CTHRC1 and Wnt/β-catenin might accelerate tumor progression. CTHRC1 serves as an essential factor in tumor development and a promising therapeutic target
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