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Fig. 11 | BMC Biology

Fig. 11

From: FGF-2 promotes angiogenesis through a SRSF1/SRSF3/SRPK1-dependent axis that controls VEGFR1 splicing in endothelial cells

Fig. 11

Graphical abstract for FGF-2-dependent regulation of sVEGFR1 splice variants in endothelial cells and its contribution to angiogenesis and lung tumorigenesis. In endothelial cells, FGF-2 stimulates a SRPK1/SRSF1/SRSF3 signaling pathway that controls VEGFR1 splicing in favor of sVEGFR1 splice variants, in particular sVEGFR1-ex12 (variant 4), that contribute to FGF-2 pro-angiogenic functions. In squamous lung carcinoma patients (LUSC), elevated sVEGFR1-ex12 usage value correlates with FGF-2/FGFR1 mRNA levels and with poor prognosis, thereby supporting a role of the FGF-2/FGFR1/sVEGFR1-ex12 signaling network in both physiological and pathological angiogenesis

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BMC Biology

ISSN: 1741-7007

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