Following our series of posts on tumour microenvironment (TME) and the role of Cox-2/PGE2 signaling, I’d like today to focus on inflammation and immunity.
TME is a dynamic milieu influenced by numerous changes favoring the emergence of a tumour-promoting inflammatory environment (eg. tissue remodeling, metabolic alterations, recruitment of stromal cells (including immune cells)…). Extracellular matrix (ECM) also participate in this inflammatory environment by promoting pro-inflammatory cytokines expression (CCL2, GM-CSF). Tumour cell progression seems to be mediated by adaptative and immune cells, where differential cytokine and chemokine expression changes the balance between Th1 (anti-tumour) and Th2 (pro-tumour) phenotypes. Microbiota also influences cancer progression by regulating the inflammatory components of TME, though how this is done needs further investigation (1).