VEGFR1 promotes cell migration and proliferation through PLCγ and PI3K pathways

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<jats:title>Abstract</jats:title><jats:p>The ability to control vascular endothelial growth factor (VEGF) signaling offers promising therapeutic potential for vascular diseases and cancer. Despite this promise, VEGF-targeted therapies are not clinically effective for many pathologies, such as breast cancer. VEGFR1 has recently emerged as a predictive biomarker for anti-VEGF efficacy, implying a functional VEGFR1 role beyond its classically defined decoy receptor status. Here we introduce a computational approach that accurately predicts cellular responses elicited via VEGFR1 signaling. Aligned with our model prediction, we show empirically that VEGFR1 promotes macrophage migration through PLC<jats:sub>γ</jats:sub> and PI3K pathways and promotes macrophage proliferation through a PLC<jats:sub>γ</jats:sub> pathway. These results provide new insight into the basic function of VEGFR1 signaling while offering a computational platform to quantify signaling of any receptor.</jats:p>

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