| http://purl.uniprot.org/citations/18372920 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18372920 | http://www.w3.org/2000/01/rdf-schema#comment | "MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively control expression of target genes in animals and plants. The microRNA-21 gene (mir-21) has been identified as the only miRNA commonly overexpressed in solid tumors of the lung, breast, stomach, prostate, colon, brain, head and neck, esophagus and pancreas. We initiated a screen to identify miR-21 target genes using a reporter assay and identified a potential miR-21 target in the 3'-UTR of the programmed cell death 4 (PDCD4) gene. We cloned the full-length 3'-UTR of human PDCD4 downstream of a reporter and found that mir-21 downregulated, whereas a modified antisense RNA to miR-21 upregulated reporter activity. Moreover, deletion of the putative miR-21-binding site (miRNA regulatory element, MRE) from the 3'-UTR of PDCD4, or mutations in the MRE abolished the ability of miR-21 to inhibit reporter activity, indicating that this MRE is a critical regulatory region. Western blotting showed that Pdcd4 protein levels were reduced by miR-21 in human and mouse cells, whereas quantitative real-time PCR revealed little difference at the mRNA level, suggesting translational regulation. Finally, overexpression of mir-21 in MCF-7 human breast cancer cells and mouse epidermal JB6 cells promoted soft agar colony formation by downregulating Pdcd4 protein levels. The demonstration that miR-21 promotes cell transformation supports the concept that mir-21 functions as an oncogene by a mechanism that involves translational repression of the tumor suppressor Pdcd4."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.org/dc/terms/identifier | "doi:10.1038/onc.2008.72"xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Li Y."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Liu M."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Lu Z."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Ramos K.S."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Colburn N.H."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Stribinskis V."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/author | "Klinge C.M."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/pages | "4373-4379"xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/title | "MicroRNA-21 promotes cell transformation by targeting the programmed cell death 4 gene."xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://purl.uniprot.org/core/volume | "27"xsd:string |
| http://purl.uniprot.org/citations/18372920 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18372920 |
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