Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis.

Yang L, DeBusk LM, Fukuda K, Fingleton B, Green-Jarvis B, Shyr Y, Matrisian LM, Carbone DP, Lin PC
Cancer Cell. 2004 6 (4): 409-21

PMID: 15488763 · DOI:10.1016/j.ccr.2004.08.031

We demonstrate a novel tumor-promoting role of myeloid immune suppressor Gr+CD11b+ cells, which are evident in cancer patients and tumor-bearing animals. These cells constitute approximately 5% of total cells in tumors. Tumors coinjected with Gr+CD11b+ cells exhibited increased vascular density, vascular maturation, and decreased necrosis. These immune cells produce high levels of MMP9. Deletion of MMP9 in these cells completely abolishes their tumor-promoting ability. Gr+CD11b+ cells were also found to directly incorporate into tumor endothelium. Consistent with this observation, Gr+CD11b+ cells acquire endothelial cell (EC) properties in tumor microenvironment and proangiogenic culture conditions. Our data provide evidence that Gr+CD11b+ cells of immune origin induced by tumors directly contribute to tumor growth and vascularization by producing MMP9 and differentiating into ECs.

MeSH Terms (19)

Animals Apoptosis Bone Marrow CD11b Antigen Cell Differentiation Cells, Cultured Disease Progression Endothelium Female Humans Matrix Metalloproteinase 9 Mice Mice, Knockout Necrosis Neoplasms Neoplasm Transplantation Neovascularization, Pathologic Stem Cell Factor Vascular Endothelial Growth Factor A

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