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• W2159956893 abstract "Signaling through vascular endothelial growth factor C (VEGF–C) and VEGF receptor 3 (VEGFR-3) plays a central role in lymphangiogenesis and the metastasis of several cancers via the lymphatics. Recently, the Slit2/Robo4 pathway has been recognized as a modulator of vascular permeability and integrity. Signaling via the Robo receptor inhibits VEGF-mediated effects; however, its effects on lymphatic endothelial cell function have not been well characterized.We found that pretreatment with Slit2N, an active fragment of Slit2, inhibited VEGF-C-mediated lung-derived lymphatic endothelial cell (L-LEC) proliferation, migration, and in vitro tube formation. Slit2N induced the internalization of VEGFR-3, which blocked its activation, and inhibited the activation of the PI3K/Akt pathway by VEGF-C in L-LECs. Moreover, we found that inhibition of VEGF-C-induced effects by Slit2N was Robo4-dependent.These results indicate that Slit2N/Robo4 modulates several key cellular functions, which contribute to lymphangiogenesis, and identify this ligand-receptor pair as a potential therapeutic target to inhibit lymphatic metastasis of VEGF-C-overexpressing cancers and manage lymphatic dysfunctions characterized by VEGF-C/VEGFR-3 activation." @default.
• W2159956893 created "2016-06-24" @default.
• W2159956893 creator A5002672292 @default.
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• W2159956893 creator A5049975962 @default.
• W2159956893 creator A5052897084 @default.
• W2159956893 creator A5073353369 @default.
• W2159956893 date "2014-04-07" @default.
• W2159956893 modified "2023-09-23" @default.
• W2159956893 title "Slit2N and Robo4 regulate lymphangiogenesis through the VEGF-C/VEGFR-3 pathway" @default.
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• W2159956893 doi "https://doi.org/10.1186/1478-811x-12-25" @default.
• W2159956893 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4122147" @default.
• W2159956893 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24708522" @default.
• W2159956893 hasPublicationYear "2014" @default.
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