TECK/CCL25 Protein, Human

CCL25, also known as thymus-expressing chemokine TECK, a small cell factor of the CC chemokine family, is located on chromosome 19 in the human genome. CCL25 is mainly expressed in the thymus and intestinal epithelium, but can also be produced by parenchymal cells such as vascular endothelial cells, which can migrate immature T cells to the thymus for mature release. It is chemotactic for thymocytes, macrophages and dendritic cells and can act in combination with the chemokine receptor CCR9. Among others, CCR9 is found as a G protein-coupled receptor expressed on the cell membranes of dendritic cells, neutrophils, lymphocytes, monocyte macrophages and vascular endothelial cells. CCR9 belongs to the β-chemokine receptor family and the gene is located on chromosome 3 at p21.31. CCL25-CCR9 is involved in the development of T cells and cell migration to the small intestine, as well as in a variety of inflammatory diseases and promotes inflammatory responses, including cardiovascular disease (CVD), hepatitis, and arthritis. The interaction of CCL25 with CCR9 also supports T cell survival during thymic maturation by inhibiting apoptosis through Akt/protein kinase B activation^[1][2].

CCL25 (100 ng/mL) can induce migration and invasion in human OvCa cell lines that are CCR9-dependent. It causes OVCAR-3 cells to significantly express MMP-8 and MMP-13 mRNA and MMP-1 and -8 active proteins, resulting in a selective but significant increase in active MMP-3 and -10 secretion by CAOV-3 cells^[3].
CCL25 (100 ng/mL) significantly enhances the growth of human BrCa cell lines MDA-MB-231 cells and protects against cisplatin (<5 μg/mL)-mediated growth inhibition. CCL25-mediated protection against cisplatin-induced growth inhibition of BrCa cells disappears as cisplatin concentrations reached ≥10 μg/mL. It also significantly reduces the percentage of apoptotic cells treated with cisplatin^[4].