| http://purl.uniprot.org/citations/21680174 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21680174 | http://www.w3.org/2000/01/rdf-schema#comment | "Vascular endothelial growth factor C (VEGF-C) expression is associated with the malignant tumour phenotype making it an attractive therapeutic target. We investigated the biological roles of VEGF-C in tumour growth, migration, invasion and explored the possibility of VEGF-C as a potential therapeutic target for the treatment of non-small cell lung cancer (NSCLC). A lentivirus-mediated RNA interference (RNAi) technology was used to specifically knockdown the expression of VEGF-C in A549 cells. Quantitative reverse transcriptase-polymerase chain reaction, flow cytometry, Western blot, immunohistochemistry, cellular growth, migration, invasion and ELISA assays were used to characterise VEGF-C expression in vitro. A lung cancer xenograft model in nude mice was established to investigate whether knockdown of VEGF-C reduced tumour growth in vivo. Silencing of VEGF-C suppressed tumour cell growth, migration and invasion in vitro; suppressed tumour growth, angiogenesis and lymphangiogenesis by tail vein injection of lentivirus encoded shRNA against VEGF-C in vivo. More importantly, silencing of VEGF-C also trapped the VEGFR-2, VEGFR-3, CXCR4, CCR7-dependent axes, and down-regulated the AKT, ERK and p38 signalling pathways. These results suggest that VEGF-C has a multifaceted role in NSCLC growth, migration and invasion; that VEGF-C-mediated autocrine loops with their cognate receptors and chemokine receptors are significant factors affecting tumour progression; and that RNAi-mediated silencing of VEGF-C represents a powerful therapeutic approach for controlling NSCLC growth and metastasis."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ejca.2011.05.006"xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Feng Y."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Hu J."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Ma J."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Zhang J."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Wang W."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Yang S."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/author | "Feng K."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/name | "Eur J Cancer"xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/pages | "2353-2363"xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/title | "RNAi-mediated silencing of VEGF-C inhibits non-small cell lung cancer progression by simultaneously down-regulating the CXCR4, CCR7, VEGFR-2 and VEGFR-3-dependent axes-induced ERK, p38 and AKT signalling pathways."xsd:string |
| http://purl.uniprot.org/citations/21680174 | http://purl.uniprot.org/core/volume | "47"xsd:string |
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| http://purl.uniprot.org/uniprot/#_A0A0H4A774-mappedCitation-21680174 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21680174 |
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