Recombinant Human CXCL14 (BRAK) (carrier-free)

CXCL14 was initially cloned from breast and kidney cells, and it is expressed at high levels and ubiquitously in normal tissue. CXCL14 is well conserved between humans, birds, frogs and fish at the amino acid level, and human and mouse CXCL14 share 95% identity. Original studies showed a decrease in the expression of CXCL14 in head and neck squamous cell carcinoma (HNSCC) and cervical squamous cell carcinoma (SCCs) tumors, and the induction of expression of CXCL14 in human oral carcinoma prevents tumor growth of these cells in vivo. Therefore, it has been suggested that CXCL14 possesses tumor suppressing function, and it has been speculated that CXCL14 secreted by stromal cells chemoattracts iDCs (immature dendritic cells) and NK cells that activate the immune response against tumor cells. Most recent data showed that epigenetic silencing of CXCL5, CXCL12, and CXCL14 occurs in 75% of primary lung adenocarcinomas. Consequently, the low expression of CXCL14 in tumors might allow them to escape immune surveillance. Opposite of HNSCC and SCCs tumors, prostate, pancreatic, and colorectal cancers show high expression of CXCL14, inducing growth and invasiveness of pancreatic and breast cancer cells.