Tumor Cell Resistance to Complement-Mediated Lysis

摘要: Complement-mediated tumor cell lysis is hampered by several protective mechanisms. Basal mechanisms of resistance are constitutively expressed in cells without a need for prior activation. These include the (over)expression membrane-associated complement regulatory proteins, such as CD55 (DAF, Decay-Accelerating Factor), CD46 (MCP, Membrane Cofactor Protein) and CD59, on cells. To generate microenvironment, secrete soluble inhibitors express their surface ecto-proteases that degrade proteins or ecto-protein kinases which impair phosphorylation functional activity certain components. Increased sialic acid expression also confers to cancer has been correlated with increased metastatic tumors. Tumor protection can be induced augmented upon stimulation cytokines, hormones, drugs even sublytic doses other pore-forming molecules. Intracellular pathways facilitate removal membrane attack complexes repair processes. Increase cytosolic calcium ion concentration, activation protein kinase C (PKC) mitogen-activated ERK, heat shock lipid metabolism synthesis, have all implicated from attack. First attempts now being made counteract these mechanisms, including targeted neutralisation mCRP Understanding complex molecular involved basal essential development strategies interference evasion effectively targeting cytotoxic system