scholarly journals YKL-40 acts as an angiogenic factor to promote tumor angiogenesis

2013 ◽  
Vol 4 ◽  
Author(s):  
Rong Shao
Keyword(s):  
Tumor Angiogenesis ◽  
Angiogenic Factor ◽  
Promote Tumor Angiogenesis

scholarly journals Cell surface expression and secretion of heparanase markedly promote tumor angiogenesis and metastasis

2002 ◽  
Vol 99 (15) ◽  
pp. 10031-10036 ◽  
Author(s):  
O. Goldshmidt ◽  
E. Zcharia ◽  
R. Abramovitch ◽  
S. Metzger ◽  
H. Aingorn ◽  
...  
Keyword(s):  
Cell Surface ◽  
Tumor Angiogenesis ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Promote Tumor Angiogenesis

scholarly journals Apelin Controls Angiogenesis-Dependent Glioblastoma Growth

2020 ◽  
Vol 21 (11) ◽  
pp. 4179 ◽  
Author(s):  
Anne Frisch ◽  
Stefanie Kälin ◽  
Raymond Monk ◽  
Josefine Radke ◽  
Frank L. Heppner ◽  
...  
Keyword(s):  
Tumor Angiogenesis ◽  
Angiogenic Factor ◽  
Normal Brain ◽  
Loss Of Function ◽  
Direct Infusion ◽  
Tip Cells ◽  
The Brain ◽  
Additional Loss

Glioblastoma (GBM) present with an abundant and aberrant tumor neo-vasculature. While rapid growth of solid tumors depends on the initiation of tumor angiogenesis, GBM also progress by infiltrative growth and vascular co-option. The angiogenic factor apelin (APLN) and its receptor (APLNR) are upregulated in GBM patient samples as compared to normal brain tissue. Here, we studied the role of apelin/APLNR signaling in GBM angiogenesis and growth. By functional analysis of apelin in orthotopic GBM mouse models, we found that apelin/APLNR signaling is required for in vivo tumor angiogenesis. Knockdown of tumor cell-derived APLN massively reduced the tumor vasculature. Additional loss of the apelin signal in endothelial tip cells using the APLN-knockout (KO) mouse led to a further reduction of GBM angiogenesis. Direct infusion of the bioactive peptide apelin-13 rescued the vascular loss-of-function phenotype specifically. In addition, APLN depletion massively reduced angiogenesis-dependent tumor growth. Consequently, survival of GBM-bearing mice was significantly increased when APLN expression was missing in the brain tumor microenvironment. Thus, we suggest that targeting vascular apelin may serve as an alternative strategy for anti-angiogenesis in GBM.

Role of Myeloid and Other Stromal Cell Types in Tumor Angiogenesis.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. SCI-32-SCI-32
Author(s):  
Napoleone Ferrara
Keyword(s):  
Growth Factor ◽  
San Francisco ◽  
Tumor Angiogenesis ◽  
Stromal Cell ◽  
Cell Types ◽  
Angiogenic Factor ◽  
Treatment Result ◽  
Angiogenic Switch ◽  
Anti Vegf

Abstract Abstract SCI-32 Role of myeloid and other stromal cell types in tumor angiogenesis Napoleone Ferrara Genentech, Inc, 1 DNA Way, South San Francisco, CA, 94080, USA. Vascular endothelial growth factor (VEGF)-A is an important angiogenic factor, involved in both physiological and pathological growth of blood vessels. An anti-VEGF-A monoclonal antibodies and two small molecule VEGF RTK inhibitors have been approved by the FDA for cancer therapy. We have been investigating the mechanisms of refractoriness/resistance to anti-VEGF therapies. Our analysis points to the mobilization and recruitment of CD11b+ Gr1+myeloid cells from the bone marrow in the tumor as key mechanisms for VEGF-independent angiogenesis, at least in mouse models. Tumors that are refractory to anti-VEGF treatment result in increased peripheral mobilization and tumor homing of of CD11b+Gr1+ cells compared to sensitive tumors. Addition of CD11b+Gr1+ cells from resistant tumors was able to sustain the growth of sensitive tumors in the presence of anti-VEGF antibodies. In subsequent studies, we identified the secreted protein Bv8 as a mediator of myeloid cell-dependent angiogenesis. Blocking Bv8 using neutralizing antibodies inhibited the growth of several tumor cell lines transplanted in nude mice and also reduced the angiogenic switch in the RIP-Tag, a transgenic model of insulinoma. The expression of Bv8 by CD11b+ Gr1+myeloid was regulated by hematopoietic growth factor, especially G-CSF. Other studies have implicated tumor-associated fibroblasts as a source of alternative pro-angiogenic factors following VEGF blockade. We identified PDGF-C as one of such mediators. In summary, multiple stromal cell types and signaling pathways may contribute to inherent refractoriness and, potentially, acquired resistance to anti-VEGF therapies in tumors. Disclosures Ferrara: Genentech, Inc.: Employment.

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