Abstract
BackgroundSrc-related kinase lacking C-terminal regulatory tyrosine and N-terminal myristoylation sites (SRMS) is a non-receptor tyrosine kinase that has been found to be overexpressed in various tumors. However, the role of SRMS in colorectal cancer (CRC) has not been well established.MethodsWe evaluated the expression levels of SRMS in CRC using GEPIA, Oncomine, and HPA datasets. Survival information and gene expression data of CRC were obtained from The Cancer Genome Atlas (TCGA). Then, the association between SRMS and clinicopathological features was analyzed using UALCAN dataset. LinkedOmics was used to determine co-expression and functional networks associated with SRMS. Besides, we used TISIDB to assess the correlation between SRMS and immune signatures, including tumor-infiltrating immune cells and immunomodulators. Lastly, protein-protein interaction network (PPI) was established and the function enrichment analysis of the SRMS-associated immunomodulators and immune cell marker genes were performed using the STRING portal.ResultsCompared to normal colorectal tissues, SRMS was found to be overexpressed in CRC tissues, which was correlated with a poor prognosis. In colon adenocarcinoma (COAD), the expression levels of SRMS are significantly correlated with pathological stages and nodal metastasis status. Functional network analysis suggested that SRMS regulates intermediate filament-based processes, protein autophosphorylation, translational initiation, and elongation signaling through pathways involving ribosomes, proteasomes, oxidative phosphorylation, and DNA replication. In addition, SRMS expression was correlated with infiltrating levels of CD4+ T cells, CD56dim, MEM B, Neutrophils, Th2, Th17, and Act DC. The gene ontology (GO) analysis of SRMS-associated immunomodulators and immune cell marker genes showed that they were mainly enriched in the immune microenvironment molecule-related signals. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of these genes indicated that they are involved in multiple cancer-related pathways.ConclusionsSRMS is a promising prognostic biomarker and potential therapeutic target for CRC patients. In particular, SRMS regulates CRC progression by modulating cytokine-cytokine receptor interaction, chemokines, IL-17, and intestinal immune networks for IgA production signaling pathways among others. However, more studies are needed to validate these findings.
Highlights
colorectal cancer (CRC) is one of the most prevalent malignancies and the fourth leading cause of cancer-related mortality, resulting in almost 900,000 annual mortality [1]
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A higher SRMS expression level was significantly associated with late TNM stages, more lymph node metastasis in colon adenocarcinoma (COAD), but not with age, gender, race, histological
Summary
CRC is one of the most prevalent malignancies and the fourth leading cause of cancer-related mortality, resulting in almost 900,000 annual mortality [1]. The high incidence of colorectal cancer is correlated with age, diet, race, lifestyle, genetic alteration, and other factors. The major therapeutic options for CRC include surgery, chemotherapy, radiotherapy, biotherapy, and immunotherapy. The 5-year survival outcomes for advanced CRC patients are approximately 10% [3, 4]. Identification of genes associated with tumor formation and metastasis will provide new ideas and targets for anti-CRC therapy. Src-related kinase lacking C-terminal regulatory tyrosine and N-terminal myristoylation sites (SRMS) is a non-receptor tyrosine kinase that has been found to be overexpressed in various tumors. The role of SRMS in colorectal cancer (CRC) has not been well established
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