| http://purl.uniprot.org/citations/31758648 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31758648 | http://www.w3.org/2000/01/rdf-schema#comment | "The vascular endothelial growth factor receptor-1 (VEGFR-1) is a tyrosine kinase receptor frequently expressed in melanoma. Its activation by VEGF-A or placental growth factor (PlGF) promotes tumour cell survival, migration and invasiveness. Moreover, VEGFR-1 stimulation contributes to pathological angiogenesis and induces recruitment of tumour-associated macrophages. Since melanoma acquired resistance to BRAF inhibitors (BRAFi) has been associated with activation of pro-angiogenic pathways, we have investigated VEGFR-1 involvement in vemurafenib resistance. Results indicate that human melanoma cells rendered resistant to vemurafenib secrete greater amounts of VEGF-A and express higher VEGFR-1 levels compared with their BRAFi-sensitive counterparts. Transient VEGFR-1 silencing in susceptible melanoma cells delays resistance development, whereas in resistant cells it increases sensitivity to the BRAFi. Consistently, enforced VEGFR-1 expression, by stable gene transfection in receptor-negative melanoma cells, markedly reduces sensitivity to vemurafenib. Moreover, melanoma cells expressing VEGFR-1 are more invasive than VEGFR-1 deficient cells and receptor blockade by a specific monoclonal antibody (D16F7 mAb) reduces extracellular matrix invasion triggered by VEGF-A and PlGF. These data suggest that VEGFR-1 up-regulation might contribute to melanoma progression and spreading after acquisition of a drug-resistant phenotype. Thus, VEGFR-1 inhibition with D16F7 mAb might be a suitable adjunct therapy for VEGFR-1 positive tumours with acquired resistance to vemurafenib."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.org/dc/terms/identifier | "doi:10.1111/jcmm.14755"xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Ruffini F."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Graziani G."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Lacal P.M."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Tentori L."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Trapani M."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Ceci C."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "D'Atri S."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Barbaccia M.L."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/author | "Atzori M.G."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/name | "J Cell Mol Med"xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/pages | "465-475"xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/title | "Role of VEGFR-1 in melanoma acquired resistance to the BRAF inhibitor vemurafenib."xsd:string |
| http://purl.uniprot.org/citations/31758648 | http://purl.uniprot.org/core/volume | "24"xsd:string |
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