http://purl.uniprot.org/citations/25257729 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25257729 | http://www.w3.org/2000/01/rdf-schema#comment | "The p53 tumor suppressor protein is primarily known for its important role in tumor suppression. In addition, p53 affects tumor cell migration, invasion, and epithelial-mesenchymal transition (EMT); processes also regulated by the transforming growth factor-β (TGF-β) signaling pathway. Here, we investigated the role of p53 in breast tumor cell invasion, migration, and EMT and examined the interplay of p53 with TGF-β3 in these processes. MCF-10A1 and MCF-10CA1a breast cancer cells were treated with Nutlin-3 and TGF-β3, and the effects on tumor cell migration and invasion were studied in transwell and 3D spheroid invasion assays. The effects of Nutlin-3 and TGF-β3 on EMT were examined in NMuMG cells. To identify genes involved in TGF-β-induced invasion that are modulated by p53, a Human Tumor Metastasis-specific RT-PCR array was performed. Verification of EPHB2 regulation by TGF-β3 and p53 was performed on breast cancer tumor cell lines. We demonstrate that p53 inhibits basal and TGF-β3-induced invasion, migration, and EMT in normal breast epithelial and breast cancer cells. Pharmacological activation of p53 inhibited induction of several TGF-β3 targets involved in TGF-β3-induced tumor cell invasion, i.e., matrix metallo proteinase (MMP)2, MMP9, and integrin β 3 . The ephrin-type B receptor 2 (EPHB2) gene was identified as a new TGF-β target important for TGF-β3-mediated invasion and migration, whose transcriptional activation by TGF-β3 is also inhibited by p53. The results show an intricate interplay between p53 and TGF-β3 whereby p53 inhibits the TGF-β3-induced expression of genes, e.g., EPHB2, to impede tumor cell invasion and migration."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.org/dc/terms/identifier | "doi:10.1007/s10549-014-3147-8"xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "ten Dijke P."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "Lam S."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "Jochemsen A.G."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "Wiercinska E."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "Teunisse A.F."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/author | "Lodder K."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/name | "Breast Cancer Res Treat"xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/pages | "7-18"xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/title | "Wild-type p53 inhibits pro-invasive properties of TGF-beta3 in breast cancer, in part through regulation of EPHB2, a new TGF-beta target gene."xsd:string |
http://purl.uniprot.org/citations/25257729 | http://purl.uniprot.org/core/volume | "148"xsd:string |
http://purl.uniprot.org/citations/25257729 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25257729 |
http://purl.uniprot.org/citations/25257729 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25257729 |
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