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- Title
Bv8 regulates myeloid-cell-dependent tumour angiogenesis.
- Authors
Farbod Shojaei; Xiumin Wu; Cuiling Zhong; Lanlan Yu; Xiao-Huan Liang; Yao, Jenny; Blanchard, Dominique; Bais, Carlos; Peale, Franklin V.; van Bruggen, Nicholas; Ho, Calvin; Ross, Jed; Tan, Martha; Carano, Richard A. D.; Meng, Y. Gloria; Ferrara, Napoleone
- Abstract
Bone-marrow-derived cells facilitate tumour angiogenesis, but the molecular mechanisms of this facilitation are incompletely understood. We have previously shown that the related EG-VEGF and Bv8 proteins, also known as prokineticin 1 (Prok1) and prokineticin 2 (Prok2), promote both tissue-specific angiogenesis and haematopoietic cell mobilization. Unlike EG-VEGF, Bv8 is expressed in the bone marrow. Here we show that implantation of tumour cells in mice resulted in upregulation of Bv8 in CD11b+Gr1+ myeloid cells. We identified granulocyte colony-stimulating factor as a major positive regulator of Bv8 expression. Anti-Bv8 antibodies reduced CD11b+Gr1+ cell mobilization elicited by granulocyte colony-stimulating factor. Adenoviral delivery of Bv8 into tumours was shown to promote angiogenesis. Anti-Bv8 antibodies inhibited growth of several tumours in mice and suppressed angiogenesis. Anti-Bv8 treatment also reduced CD11b+Gr1+ cells, both in peripheral blood and in tumours. The effects of anti-Bv8 antibodies were additive to those of anti-Vegf antibodies or cytotoxic chemotherapy. Thus, Bv8 modulates mobilization of CD11b+Gr1+ cells from the bone marrow during tumour development and also promotes angiogenesis locally.
- Subjects
NEOVASCULARIZATION; TUMOR growth; BONE marrow diseases; CANCER cells; IMMUNOGLOBULINS; NEOVASCULARIZATION inhibitors; DRUG therapy; GENE expression; GRANULOCYTES
- Publication
Nature, 2007, Vol 450, Issue 7171, p825
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/nature06348