| http://purl.uniprot.org/citations/21706045 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21706045 | http://www.w3.org/2000/01/rdf-schema#comment | "Fusion proteins containing the amino terminus of mixed lineage leukemia (MLL) are common in acute lymphoblastic leukemia (ALL) due to translocations. The MLL-AF4 fusion protein is generated by the translocation t(4;11)(q21;q23), and t(4;11)-positive ALL patients (MLL-AF4 ALL), have a notoriously poorer prognosis compared with patients with other MLL-associated leukemias. The detailed role of this fusion protein in leukemogenesis is not well understood. MicroRNAs (miRNAs) targeting the AF4 3' untranslated regions may modulate MLL-AF4 fusion protein levels, raising the question of whether regulation of these miRNAs are involved in the progression of MLL-AF4 ALL. In this study, we show that miR-143 was identified as a regulator of MLL-AF4 expression in MLL-AF4 ALL samples. Restoration of miR-143 in MLL-AF4-positive RS4;11 and MV4-11 cells induced apoptosis, negatively contributing to leukemia cell growth by reducing MLL-AF4 fusion protein levels. Furthermore, miR-143 was epigenetically repressed by promoter hypermethylation in MLL-AF4-positive primary blasts and cell lines, but not in normal bone marrow cells and MLL-AF4-negative primary blasts, which was directly associated with expression of the MLL-AF4 oncogene. This is the first study to show that miR-143 functions as a tumor suppressor in MLL-AF4 B-cell ALL. These data reveal the therapeutic promise of upregulating miR-143 expression for MLL-AF4 B-cell ALL."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.org/dc/terms/identifier | "doi:10.1038/onc.2011.248"xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Gao L."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Li Y."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Yu L."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Zheng D."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/author | "Dou L."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/pages | "507-517"xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/title | "Methylation-mediated repression of microRNA-143 enhances MLL-AF4 oncogene expression."xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://purl.uniprot.org/core/volume | "31"xsd:string |
| http://purl.uniprot.org/citations/21706045 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21706045 |
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