Abstract
The epithelial-mesenchymal transition (EMT) process is tightly connected to tumors' immune microenvironment. In colon adenocarcinoma (COAD), both the EMT and immune cell infiltration contribute to tumor progression; however, several questions regarding the mechanisms governing the interaction between EMT and the immune response remain unanswered. Our study aims to investigate the cross-talk between these two processes in cases of COAD and identify the key regulators involved. We utilized the EMT and immune signatures of samples from the COAD-TCGA database to identify three subtypes of COAD: high mesenchymal, medium mesenchymal, and low mesenchymal. We observed that EMT was associated with increased tumor immune response and infiltration mediated by pro-inflammatory cytokines. However, EMT was also linked to immunosuppressive activity that involved regulatory T cells, dendritic cells, and the upregulated expression of multiple immune checkpoints, such as PD-1, PDL-1, CTLA-4, and others. Finally, we employed the multivariate random forest feature importance method to identify key genes, such as DOK2 and MSRB3, that may play crucial roles in both EMT and the intratumoral immune response.