| http://purl.uniprot.org/citations/26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26134542 | http://www.w3.org/2000/01/rdf-schema#comment | "In recent years, astrocyte elevated gene-1 (AEG-1) has been reported as a key mediator that is involved in the epithelial-to-mesenchymal transition (EMT) process. However, the mechanisms underlying CCL3/CCR5-AEG-1 pathway-mediated EMT in cardiac myxoma (CM) has not been well featured till now. We used immnohistochemistry and immunoblotting to assess the expression of CCR5 and AEG-1 in 30 cases of CM tissues and cells. Subsequently, cultured CM cells were treated with si-AEG-1 or si-CCR5 and then subjected to in vitro assays. We observed that CCR5 and AEG-1 proteins were highly expressed in CM tissues (73.3 and 76.7%, respectively) and closely correlated with tumor size (>5 cm). Importantly, we validated the expression of AEG-1, p-Erk1/2, p-Akt, vimentin, N-cadherin and MMP2 increased in the CM cell with CCL3 treatment in a time-and concentration-dependent manner. When CM cells were treated with si-CCR5, the expression of AEG-1, p-Erk1/2, p-Akt, vimentin, N-cadherin and MMP2 was downregulated. In addition, when CM cells were treated with si-AEG-1, the expression of p-Erk1/2, p-Akt, vimentin, N-cadherin and MMP2 was also downregulated. Using the cell cycle and proliferation assay, the knockdown of AEG-1 inhibited the entry of G1 into S phase and the proliferation capacity of CM cells. In conclusion, AEG-1 mediates CCL3/CCR5-induced EMT development via both Erk1/2 and Akt signaling pathway in CM patients, which indicates CCL3/CCR5-AEG-1-EMT pathway could be suggested as a useful target to affect the progression of CM."xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.org/dc/terms/identifier | "doi:10.3892/or.2015.4081"xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/author | "Pang X."xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/author | "Fang C."xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/author | "Shi P."xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/name | "Oncol Rep"xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/pages | "1319-1326"xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/title | "Astrocyte elevated gene-1 regulates CCL3/CCR5-induced epithelial-to-mesenchymal transition via Erk1/2 and Akt signaling in cardiac myxoma."xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://purl.uniprot.org/core/volume | "34"xsd:string |
| http://purl.uniprot.org/citations/26134542 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26134542 |
| http://purl.uniprot.org/citations/26134542 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G6S6-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G6S9-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G7F7-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G7G0-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G7G7-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G7G9-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G3J8-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G3N4-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G3P0-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G3P4-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G5M8-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |
| http://purl.uniprot.org/uniprot/#_A0A089G5N2-mappedCitation-26134542 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26134542 |