The present study aims to identify immune-related prognostic genes in colorectal cancer (CRC), and to explore potential mechanisms through which these genes regulate CRC progression. We first constructed a prognostic risk model based on seven gene signatures [cluster of differentiation-36 (CD36), chemokine (C-X-C-motif) ligand 13 (CXCL13), fibroblast growth factor receptor 4 (FGFR4), gamma-amino-butyric acid type B receptor 1 (GABBR1), lysosome-associated membrane glycoprotein 3 (LAMP3), recombinant matrix metalloproteinase 12 (MMP12), and protein phosphatase 1H (PPM1H)] using integrated bioinformatic analyses. FGFR4, GABBR1, and LAMP3 were highly expressed in CRC cell lines (in comparison with a normal colonic epithelial cell line), while CD36, CXCL13, MMP12, and PPM1H were weakly expressed. These in vitro expression results were largely consistent with our bioinformatic analysis. A prognostic model was generated to identify a high-risk group with worse survival outcome based on Kaplan-Meier analysis. Our prognostic model showed superior accuracy in both the training and test cohorts. In addition, we found that the low-risk subgroup exhibited greater infiltration by M1 macrophages, CD8+ T cells, CD4+ T cells, and activated NK cells. In conclusion, our findings provide evidence that seven immune-related hub genes can be considered as gene signatures to predict CRC prognosis and to differentiate CRC patient benefit, ultimately serving as a guide for individualized immunotherapy.
Keywords: Colorectal cancer; immune cell infiltration; prognostic biomarkers; tumor immune microenvironment.
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