2012
DOI: 10.1074/jbc.m111.326801
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Induction of Bv8 Expression by Granulocyte Colony-stimulating Factor in CD11b+Gr1+ Cells

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Cited by 80 publications
(68 citation statements)
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“…44,45 G-CSF is also a potent inducer of PROK2-expression in vitro and in vivo through STAT3 signaling. 42,46,47 However, neither IL6 nor IL10 triggers the expression of PROK2, 46 suggesting that these interleukins do not stimulate PROK2-expression following GR, which is consistent with our findings of increased IL6 expression (Fig. 2A).…”
Section: Methodssupporting
confidence: 90%
“…44,45 G-CSF is also a potent inducer of PROK2-expression in vitro and in vivo through STAT3 signaling. 42,46,47 However, neither IL6 nor IL10 triggers the expression of PROK2, 46 suggesting that these interleukins do not stimulate PROK2-expression following GR, which is consistent with our findings of increased IL6 expression (Fig. 2A).…”
Section: Methodssupporting
confidence: 90%
“…Interestingly, Th17 cells produce the cytokine IL17, whose role in promoting tumor resistance to antiangiogenic therapy has begun to unravel recently (36). In addition, multiple myeloid-derived inflammatory mediators have been shown to mediate resistance to anti-VEGF therapy in preclinical models (36)(37)(38). Understanding how everolimus regulates OPN in these specific cell populations, and the consequences of intracellular versus soluble OPN (39), is of great interest.…”
Section: Discussionmentioning
confidence: 99%
“…This effect of G-CSF is mediated through recruitment of CD11b + Gr1 + MDSCs and increased number of endothelial progenitor cells [279]. The pro-angiogenic effects of MDSCs is in part driven by Bv8 (prokineticin 2/PK2), which is upregulated by G-CSF [282,283] through a STAT3 dependent mechanism [284]. G-CSF may further contribute to tumor angiogenesis by inducing VEGF-A production in neutrophils [285].…”
Section: Neutrophils At the Primary Tumor Sitementioning
confidence: 99%