cad a22 4500 317039601 20181103074222.0 cr unu---uuuuu 140621s2014 xx s 000 0 eng 10.1038/onc.2013.272 doi 10.1038/onc.2013.272 doi (ZORA)oai:www.zora.uzh.ch:85253 (ZORA)oai:www.zora.uzh.ch:86002 610 ddc 570 ddc 23851506 pmid Inflammatory chemokines and metastasis-tracing the accessory [Elektronische Daten] [L Borsig, M J Wolf, M Roblek, A Lorentzen, M Heikenwalder] closedAccess eu-repo The tumor microenvironment consists of stromal cells and leukocytes that contribute to cancer progression. Cross-talk between tumor cells and their microenvironment is facilitated by a variety of soluble factors, including growth factors and cytokines such as chemokines. Due to a wide expression of chemokine receptors on cells in the tumor microenvironment, including tumor cells, chemokines affect various processes such as leukocyte recruitment, angiogenesis, tumor cell survival, tumor cell adhesion, proliferation, vascular permeability, immune suppression, invasion and metastasis. Inflammatory chemokines are instrumental players in cancer-related inflammation and significantly contribute to numerous steps during metastasis. Recruitment of myeloid-derived cells to metastatic sites is mainly mediated by the inflammatory chemokines CCL2 and CCL5. Tumor cell homing and extravasation from the circulation to distant organs are also regulated by inflammatory chemokines. Recent experimental evidence demonstrated that besides leukocyte recruitment, tumor cell-derived CCL2 directly activated endothelial cells and together with monocytes facilitated tumor cell extravasation, in a CCL2- and CCL5-dependent manner. Furthermore, CX3CL1 expression in the bone facilitated metastasis of CX3CR1 expressing tumor cells to this site. Current findings in preclinical models strongly suggest that inflammatory chemokines have an important role during metastasis and targeting of the chemokine axis might have a therapeutic potential.Oncogene advance online publication, 15 July 2013; doi:10.1038/onc.2013.272. Center for Integrative Human Physiology zora Institute of Physiology zora Borsig L. joint author Wolf M J. joint author Roblek M. joint author Lorentzen A. joint author Heikenwalder M. joint author Oncogene 33(25):3217-3224 https://www.zora.uzh.ch/85253 text/html WWW-Backlink auf das Repository 1 Journal Article PeerReviewed zora ZORA 856 40 https://www.zora.uzh.ch/85253 text/html WWW-Backlink auf das Repository ZORA 700 1- Wolf M J. joint author ZORA 700 1- Roblek M. joint author ZORA 700 1- Heikenwalder M. joint author ZORA 700 1- Borsig L. joint author ZORA 700 1- Lorentzen A. joint author ZORA 773 0- Oncogene 33(25):3217-3224 ZORA 700 1- Roblek Marko joint author ZORA 856 40 https://www.zora.uzh.ch/id/eprint/86002/1/Borsig_et_al_Oncogene_in_press.pdf text/html WWW-Backlink auf das Repository ZORA 700 1- Heikenwalder Mathias joint author ZORA 700 1- Wolf Monika Julia joint author BK010053 XK010053 XK010000 ZORA ZORA ZORA Journal Article closedAccess ZORA ZORA ZORA Journal Article openAccess