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- W2519602258 abstract "Neuropilin-1 (NP1), originally identified as a receptor for the semaphorin/collapsin family of neuronal mediators, has recently been documented as an isoform-specific receptor for VEGF165 on a number of tumour cell types. At present, it is unclear as to the mechanism of NP1 signalling in lung tumour cells. We investigated the role of the phosphatidylinositol-3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) cell signalling pathways in hypoxic lung tumour cells and the effect of blocking the NP1 receptor on these survival pathways. We have previously shown that NP1 and vascular endothelial growth factor (VEGF) are expressed in the non-small cell lung cancer cells, H647, A549 and SKMES1, at the mRNA and protein levels by RT-PCR and Western blotting, respectively. Phosphorylated levels of the downstream cell signalling proteins of the PI3K (phosphatidylinositol 3-kinase) and MAPK (mitogen-activated protein kinase) pathways, Akt and Erk1/2, respectively, were examined in lung tumour tissues relative to their matched normal tissue. A549 (adenocarcinoma) and SKMES1 (squamous cell carcinoma) cells were treated with a neutralising antibody to NP1 (1μg/ml) under hypoxia (0.1% O2), in the presence or absence of recombinant human VEGF (100ng/ml). Expression levels of phospho-Akt and phospho-Erk1/2 were examined by Western blot. Expression levels and localisation of both phosphorylated proteins in response to NP1 blockade under hypoxia, were examined in A549 and SKMES1 cells using the Cellomics™ IN Cell Analyzer 1000. Apoptosis was assessed by Flow Cytometry using AnnexinV/Propidium Iodide staining. In a panel of adenocarcinoma and squamous cell lung carcinomas from a series of lung cancer patients, pAkt and pErk1/2 levels were overexpressed relative to their matched normal tissues. In A549 and SKMES1 cell lines, hypoxia increased phospho-Akt relative to cells grown under normoxia. Inclusion of NP1 antibodies abrogated this hypoxia-induced increase in phospho-Akt in both cell lines, while a downregulation of phospho-Erk was seen in SKMES1 cells only. NP1 blockade under hypoxia significantly induced apoptosis in both cell lines relative to cells grown under normoxia and hypoxia alone. These results suggest a role for the PI3K and MAPK signalling pathways in the survival of lung tumour cells under hypoxia, an effect that can be inhibited by blocking NP1." @default.
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- W2519602258 date "2007-08-01" @default.
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- W2519602258 title "PD2-1-6: Neuropilin-1 blockade inhibits hypoxia-induced Akt and MAPK phosphorylation and induces apoptosis of non-small cell lung cancer cells" @default.
- W2519602258 doi "https://doi.org/10.1097/01.jto.0000283352.92000.77" @default.
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