Colorectal cancer (CRC), among the major cancer types in western world is responsible for 10% of cancer related deaths, often due to late detection when the tumor has already spread out of the colon. Surgery is the mainstay curative treatment for CRC. Nevertheless, between 15-30% of stage II and III patients develop hepatic metastasis within 5 years. Paradoxically, tumor surgery can contribute to the metastatic process, due to inflammatory mediator release in response to surgery, which promotes the metastatic ability of cancer cells. During surgery, bacterial products, such as LPS, from commensal bacteria translocate across the bowel wall, reach systemic circulation and induce an inflammatory response through to the activation of the Nuclear Factor-ĸB (NF-ĸB) pathway. Inflammation promotes malignant transformation by inducing chromosomal and microsatellite instability or CpG island methylation [14], but its direct effect on cancer cells and contribution to metastasis development remains to be elucidated. In this experiment we mimic the perioperative microenvironment where bacterial products get in contact with CRC cancer cells. We assessed the identity of the secreted proteins, including those released through extracellular vesicles (EV), of six CRC cell lines once exposed to lipopolysaccharide (LPS).