Key result
VEGF drives NSCLC survival and tumor growth primarily via Neuropilin-1 receptor signaling.
Why the study?
The survival benefit of current VEGF-targeted therapies in NSCLC is limited and new targeted therapies are urgently needed due to underwhelming results with tyrosine kinase inhibitors.
Population
NSCLC cell lines and nude mice xenograft models
Comparison
Inhibition of VEGF pathway and NP1 stable transfection vs controls
Design
Preclinical experimental study
Authors
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NP1 merits testing as a VEGF target in NSCLC; leaves open clinical translation from xenograft data.
p-value: p=<0.01
VEGF acts as an autocrine growth factor in NSCLC signaling through NP1, suggesting NP1 as a potential therapeutic target and biomarker for VEGF-targeted therapies.
Barr et al. (2015) studied Non-small cell lung cancer (preclinical) (n=16). VEGF pathway modulation (recombinant VEGF, neutralizing antibodies, siRNA, NP1 overexpression) vs. Control (untreated, IgG isotype, scrambled siRNA, empty vector) was evaluated on Tumor cell proliferation and in vivo tumor growth (p=<0.01). VEGF acts as an autocrine growth factor in non-small cell lung cancer, signaling primarily through the Neuropilin-1 receptor to promote cell survival and tumor growth.
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