Anti-CXCR1: Polyclonal CXCR1 Antibody

CXCL8, in addition to other cytokines such has IL-6, has been implicated in tissue inflammation and repair as well as carcinogenesis. It has been shown to be an important angiogenic factor. Both CXCR1 and CXCR2 also have been implicated in the angiogenic response and in the migration of neutrophils and lymphocytes. It has been demonstrated that Phosphatidylinositol-3 kinase (PI3K), the GTP-binding proteins Rac, Rho and cdc42 as well as phospholipase c participate in regulating CXCR1-mediated chemotaxis, and Cbl and Akt are also key components of this pathway.³ Moreover, CXCL8/CXCR1/2 may be involved in regulation of self-renewal or survival pathways incancer stem cell (CSC). CXCR1 activation upon IL-8 binding induces FAK phosphorylation. Active FAK phosphorylates AKT and activates the WNT pathway, which regulates stem cell self-renewal and FOXO3A that regulates cell survival. Activation of FAK protects CSCs from a FASL/FAS-mediated bystander effect by inhibiting FADD, a downstream effector of FAS signaling. In the presence of chemotherapy, only the bulk tumor cells are sensitive to the treatment and release a high level of IL-8 and FASL proteins during the apoptotic process. Breast CSCs are stimulated via an IL-8–mediated bystander effect and are resistant to the bystander killing effect mediated by FASL. CXCR1 blockade may provide a novel means of targeting and eliminating breast CSCs.⁴