Promotion of Tumor Invasion by Tumor-Associated Macrophages: The Role of CSF-1-Activated Phosphatidylinositol 3 Kinase and Src Family Kinase Motility Signaling.

摘要: Macrophages interact with cells in every organ to facilitate tissue development, function and repair. However, the close interaction between macrophages parenchymal can be subverted disease, particularly cancer. Motility is an essential capacity for able carry out their various roles. In cancers, macrophage’s interstitial migratory ability frequently co-opted by tumor enable escape from primary metastatic spread. Macrophage accumulation within movement through a often stimulated cell production of mononuclear phagocytic growth factor, colony-stimulating factor-1 (CSF-1). CSF-1 also regulates macrophage survival, proliferation differentiation, its many effects are transduced receptor, CSF-1R, via phosphotyrosine motif-activated signals. Mutational analysis CSF-1R signaling indicates that major mediators CSF-1-induced motility phosphatidyl-inositol-3 kinase (PI3K) one or more Src family (SFK), which activate signals adhesion, actin polymerization, polarization and, ultimately, migration invasion macrophages. The transcriptome, including machinery, very complex highly responsive environment, selective expression proteins splice variants rarely found other types. Thus, unique machinery specifically targeted block migration, thereby, inhibit metastasis.