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| http://purl.uniprot.org/citations/22406619 | http://www.w3.org/2000/01/rdf-schema#comment | "Bv8 (prokineticin 2) expressed by Gr1(+)CD11b(+) myeloid cells is critical for VEGF-independent tumor angiogenesis. Although granulocyte colony-stimulating factor (G-CSF) has been shown to be a key inducer of Bv8 expression, the basis for Bv8 production in driving tumor angiogenesis is undefined. Because the cell adhesion molecule CEACAM1, which is highly expressed on Gr1(+)CD11b(+) myeloid cells, is known to regulate G-CSF receptor (G-CSFR) signaling, we hypothesized that CEACAM1 would regulate Bv8 production in these cells. In support of this hypothesis, we found that Bv8 expression was elevated in Gr1(+)CD11b(+) cells from Ceacam1-deficient mice implanted with B16 melanoma, increasing the infiltration of Gr1(+)CD11b(+) myeloid cells in melanoma tumors and enhancing their growth and angiogenesis. Furthermore, treatment with anti-Gr1 or anti-Bv8 or anti-G-CSF monoclonal antibody reduced myeloid cell infiltration, tumor growth, and angiogenesis to levels observed in tumor-bearing wild-type (WT) mice. Reconstitution of CEACAM1-deficient mice with WT bone marrow cells restored tumor infiltration of Gr1(+)CD11b(+) cells along with tumor growth and angiogenesis to WT levels. Treatment of tumor-bearing WT mice with anti-CEACAM1 antibody limited tumor outgrowth and angiogenesis, albeit to a lesser extent. Tumor growth in Ceacam1-deficient mice was not affected significantly in Rag(-/-) background, indicating that CEACAM1 expression in T and B lymphocytes had a negligible role in this pathway. Together, our findings show that CEACAM1 negatively regulates Gr1(+)CD11b(+) myeloid cell-dependent tumor angiogenesis by inhibiting the G-CSF-Bv8 signaling pathway."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-11-3016"xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/author | "Pan H."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/author | "Lu R."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/author | "Shively J.E."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/author | "Kujawski M."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/pages | "2239-2250"xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/title | "Tumor angiogenesis mediated by myeloid cells is negatively regulated by CEACAM1."xsd:string |
| http://purl.uniprot.org/citations/22406619 | http://purl.uniprot.org/core/volume | "72"xsd:string |
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