期刊
BLOOD
卷 117, 期 23, 页码 6255-6266出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-10-315432
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资金
- Spanish Ministry of Science and Innovation (MICINN) [SAF2009-11426, SAF2007-64571, SAF2009-07973, CSD2007-00017]
- Juan de la Cierva and Ramon y Cajal
- Association for International Cancer Research [08-0188]
- Fundacion Ramon Areces, Fundacion Mutua Madrilena Automovilista
- Centro de Investigaciones Biomedicas en Red de Enfermedades Raras network from the MICINN
- Spanish National Bioinformatics Institute
- OncoCycle Program (Comunidad de Madrid) [S-BIO-0283-2006]
- European Community [HEALTH-F5-2010-241548]
Many mammalian transcripts contain target sites for multiple miRNAs, although it is not clear to what extent miRNAs may coordinately regulate single genes. We have mapped the interactions between down-regulated miRNAs and overexpressed target protein-coding genes in murine and human lymphomas. Myc, one of the hallmark oncogenes in these lymphomas, stands out as the up-regulated gene with the highest number of genetic interactions with down-regulated miRNAs in mouse lymphomas. The regulation of Myc by several of these miRNAs is confirmed by cellular and reporter assays. The same approach identifies MYC and multiple Myc targets as a preferential target of down-regulated miRNAs in human Burkitt lymphoma, a pathology characterized by translocated MYC oncogenes. These results indicate that several miRNAs must be coordinately down-regulated to enhance critical oncogenes, such as Myc. Some of these Myc-targeting miRNAs are repressed by Myc, suggesting that these tumors are a consequence of the unbalanced activity of Myc versus miRNAs. (Blood. 2011; 117(23): 6255-6266)
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