MYB transcriptionally regulates the miR-155 host gene in chronic lymphocytic leukemia
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21296997
DOI
10.1182/blood-2010-05-285064
PII: S0006-4971(20)45307-8
Knihovny.cz E-resources
- MeSH
- Chromatin chemistry genetics metabolism MeSH
- Leukemia, Lymphocytic, Chronic, B-Cell genetics metabolism MeSH
- Transcription, Genetic physiology MeSH
- HeLa Cells MeSH
- Humans MeSH
- MicroRNAs genetics MeSH
- Microarray Analysis MeSH
- Tumor Cells, Cultured MeSH
- Oncogene Proteins v-myb metabolism physiology MeSH
- Promoter Regions, Genetic MeSH
- Gene Expression Regulation, Leukemic MeSH
- Cluster Analysis MeSH
- Gene Expression Profiling MeSH
- Transfection MeSH
- Protein Binding MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chromatin MeSH
- MicroRNAs MeSH
- MIRN155 microRNA, human MeSH Browser
- Oncogene Proteins v-myb MeSH
Elevated levels of microRNA miR-155 represent a candidate pathogenic factor in chronic B-lymphocytic leukemia (B-CLL). In this study, we present evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients. MYB physically associates with the promoter of miR-155 host gene (MIR155HG, also known as BIC, B-cell integration cluster) and stimulates its transcription. This coincides with the hypermethylated histone H3K4 residue and spread hyperacetylation of H3K9 at MIR155HG promoter. Our data provide evidence of oncogenic activities of MYB in B-CLL that include its stimulatory role in MIR155HG transcription.
References provided by Crossref.org
Combined Approach to Leukemic Differentiation Using Transcription Factor PU.1-Enhancing Agents
MicroRNAs in B-cell lymphomas: how a complex biology gets more complex
