Cancer research is increasingly focusing on the tumour microenvironment (TME). Several studies have shown that tumours depend on external signals for maintenance and expansion. It is therefore needed to have a deeper knowledge of the cross-talk between tumour cells in the stroma (fibroblasts, adipocytes, endothelial cells and macrophages) and their microenvironment which also includes the study of interactions between cancer cells and cancer stem cells. TME studies also involve soluble factors, signaling molecules, extracellular matrix proteins (ECM) and other factors that help the tumour grow and invade other tissues, protect it from the host immune system, and contributes to therapeutic resistance in some cases (1). In a previous post, we discussed the role of Cox-2 signaling and PGE2 in TME. Also, we have already discussed the role of inflammation and the modification of the host’s immune response by cancer cells.
Today, we would like to focus on how TME affects the glycosylation of proteins involved in tumour progression.