Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment

摘要: Development of colorectal cancer has been considered as a result imbalance pro- and anti-inflammatory intestinal microenvironment accompanied by macrophage recruitment. Despite macrophages are implicated in remodeling tumor microenvironment, the mechanism recruitment is not fully elucidated yet. In this study, we reported clinical association highly expressed pyruvate kinase M2 with attraction. The conditioned medium from Caco-2 HT-29 cells depleted dramatically reduced recruitment, which reversed addition of, critical chemotaxis factor to migration, rCCL2. Silencing endogenous markedly decreased CCL2 expression secretion real-time quantitative polymerase chain reaction enzyme-linked immunosorbent assay. Endogenous interacted p65 mediated nuclear factor-κB signaling pathway mainly regulated phosphorylation Ser276 on factor-κB. addition, inhibition caused silencing was rescued ectopic p65. Interestingly, tissue, correction distribution. Taken together, revealed novel promoting progression through factor-κB-mediated CCL2.