C-X-C receptor type 4 promotes metastasis by activating p38 mitogen-activated protein kinase in myeloid differentiation antigen (Gr-1)-positive cells.

ABSTRACT: Increasing evidence suggests that myeloid bone marrow-derived cells (BMDCs) play a critical role in lung metastasis. Blockade of VEGF receptor 1 (VEGFR1) has been proposed as a potential strategy to limit myeloid BMDC recruitment to tumors. However, preclinical evidence indicates that this strategy may not be effective in all tumors. Thus, establishing which molecular mechanisms are responsible for the "escape" of these BMDCs from VEGFR1 inhibition would facilitate development of strategies to control metastasis. Here, we report the complementary role of the chemokine (C-X-C motif) ligand 12/C-X-C chemokine receptor 4 (CXCR4) and VEGF/VEGFR1 pathways in promoting lung metastasis in mice via BMDC recruitment using chimeric mice with deficiency in CXCR4 and VEGFR1-tyrosine kinase in the BMDC

SUBMITTER: Hiratsuka S 

PROVIDER: S-EPMC3017172 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature