The epigenetic cross-talk between tumor cells and immune microenvironment in colorectal cancer

Disruption of epigenetic processes can lead to altered gene function and malignant cellular transformation and influence the local anti-tumor immune response. In this study, we examined the relationship between the H3K27me3 and effector T-cell trafficking. We showed that H3K27me3 repress the tumor production of T helper 1 (TH1)-type chemokines CXCL9 and CXCL10, and subsequently determine effector T-cell trafficking to the tumor microenvironment. On the other hand, local trafficking in response to CCR6/CCL20 ligation is associated with increased Th22 phenotype. Th22 derived IL-22 activates DOT1L complex which turned on stem cell gene expression, increased cancer stemness, and promoted tumorigenic potential. The knowledge about the alterations in the epigenetic landscape of colorectal cancer may lead to understand colon cancer immunology and design effective treatments.