PRKCB is a novel and potential biomarker in colon cancer and shapes an inflamed tumor immune microenvironment

Abstract

Abstract Background Only a small subset of colon cancer patients with mismatch repair deficiency may also benefit from Immune checkpoint inhibitors (ICIs). New biomarkers correlated with ICIs responsiveness need to be explored. Methods The study data were obtained from TCGA, GEO, cBioPortal, UALCAN, UCSC Xena browser, and CPTAC databases. Protein kinase C beta (PRKCB) was screened via weighted gene co-expression network analysis (WGCNA), survival analysis and differential expression analysis. The biological and immune landscape of PRKCB was explored by performing bioinformatics and immunohistochemical analyses. These findings were used to predict responsiveness to immunotherapy. Results Yellow module in WGCNA, as a hub module, was strongly positively correlated with infiltrated CD8 + T cell and Immune Score. PRKCB was an essential member of the yellow module, downregulated in colon cancer tissue, and associated with poor prognosis. GO, KEGG, REACTOME enrichment analysis showed PRKCB was associated with Cytokine-cytokine receptor interaction, Chemokine signaling pathway, T cell receptor signaling pathway, NF-κB signal pathway, Natural killer cell mediated cytotoxicity, and PD-L1 signaling. Meanwhile, the PRKCB expression was highly positively correlated with the infiltration of the CD4 + T cells, CD8 + T cells, and NK cells. Moreover, the immunohistochemistry analysis of tissue microarray demonstrated that PRKCB expression was positively correlated with infiltrated CD8 + T cell and PD-L1 expression. As expected, the TIDE and SubMap algorithm verified that ICIs could be effective in PRKCB-high patients. Conclusion PRKCB-high was associated with good prognoses in colon cancer patients. PRKCB-high was an indicator of inflamed TIME, which correlated with high responsiveness to immunotherapy in colon cancer patients.