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The presence of inflammation in the tumor microenvironment is one of the hallmarks of cancer. Macrophages are immune response cells that act as modulators of inflammation, mediating different events in the inflammatory process. Because of their plasticity, they can assume different phenotypes depending on the type of stimulus and their microenvironment. In general, classically activated macrophages, or M1 macrophages, have a pro-inflammatory characteristic and production of ROS and NO, which are important for their anti-tumor profile. Alternately activated macrophages, or M2 macrophages, have anti-inflammatory properties, inducing tissue remodeling and repair. The tumor microenvironment is rich in macrophages, called TAM (tumor-associated macrophage), which have an M2 phenotype and are directly related to different stages of tumor development, modulating migration, invasion, angiogenesis and metastasis. Due to their high complexity and plasticity, therapies that focus on TAMs, particularly those that can change their profile and reprogram their functions against the tumor, are promising targets for cancer control. In previous research, our group demonstrated that lipoxin is able to modify the phenotype of TAMs, restoring their cytotoxic properties, such as the production of ROS and NO, leading to apoptosis of tumor cells. However, the work carried out so far has shown the effect of lipoxin on TAMs originating from only one tumor type, polarized with conditioned medium from MV3, a human melanoma cell line.
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