| http://purl.uniprot.org/citations/30926432 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/30926432 | http://www.w3.org/2000/01/rdf-schema#comment | "The endothelin-1 (ET-1) axis contributes to the pathophysiology of several cancers by promoting tumor development and progression. This peptide is activated from its precursor, big ET-1, by endothelin-converting enzyme-1 (ECE-1). Active ET-1 binds to its cognate G-coupled receptor, ETAR, which transduces the signal to the inside of the cell. ET-1 has a short half-life of about 90 s, so its biological effects are completely dependent on its enzymatic activation by ECE-1. Expression of ECE-1 is elevated in several tumors and cancer cell lines. There are four ECE-1 isoforms -ECE-1a, -1b, -1c, and -1d-which vary in terms of their subcellular localization and, in some cases, their effects on cancer-related properties such as proliferation and invasiveness. In this article, we review findings on the role of ECE-1, particularly isoform ECE-1c, in oncogenesis and malignant progression. We also review evidence regarding ECE-1 expression in several types of tumors and cancer cell lines. Recent findings from our laboratory and others allow us to speculate on the mechanism by which ECE-1c promotes cancer aggressiveness. Finally, we evaluate potential post-translational modifications of ECE-1c, highlighting phosphorylation by several kinases, as well as evidence pointing to a putative, non-canonical, ET-1-independent mechanism for promoting invasiveness. Taken together, current evidence suggests that ECE-1c contributes to cancer aggressiveness and plays a putative role as a key regulator of cancer progression. Therefore, we propose that this protein is a promising target for prognostic and therapeutic purposes."xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.canlet.2019.03.033"xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/author | "Tapia J.C."xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/author | "Niechi I."xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/name | "Cancer Lett"xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/pages | "152-157"xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/title | "Endothelin-converting enzyme-1 in cancer aggressiveness."xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://purl.uniprot.org/core/volume | "452"xsd:string |
| http://purl.uniprot.org/citations/30926432 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/30926432 |
| http://purl.uniprot.org/citations/30926432 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/30926432 |
| http://purl.uniprot.org/uniprot/#_B4DKB2-mappedCitation-30926432 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30926432 |
| http://purl.uniprot.org/uniprot/#_P42892-mappedCitation-30926432 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30926432 |
| http://purl.uniprot.org/uniprot/B4DKB2 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/30926432 |
| http://purl.uniprot.org/uniprot/P42892 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/30926432 |