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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2008-6-9
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pubmed:databankReference |
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pubmed:abstractText |
The mammalian genome contains several hundred microRNAs that regulate gene expression through modulation of target mRNAs. Here, we report a fragile chromosomal region lost in specific hematopoietic malignancies. This 7 Mb region encodes about 12% of all genomic microRNAs, including miR-203. This microRNA is additionally hypermethylated in several hematopoietic tumors, including chronic myelogenous leukemias and some acute lymphoblastic leukemias. A putative miR-203 target, ABL1, is specifically activated in these hematopoietic malignancies in some cases as a BCR-ABL1 fusion protein (Philadelphia chromosome). Re-expression of miR-203 reduces ABL1 and BCR-ABL1 fusion protein levels and inhibits tumor cell proliferation in an ABL1-dependent manner. Thus, miR-203 functions as a tumor suppressor, and re-expression of this microRNA might have therapeutic benefits in specific hematopoietic malignancies.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3' Untranslated Regions,
http://linkedlifedata.com/resource/pubmed/chemical/4-phenylbutyric acid,
http://linkedlifedata.com/resource/pubmed/chemical/Azacitidine,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Modification Methylases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/MicroRNAs,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylbutyrates,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-abl,
http://linkedlifedata.com/resource/pubmed/chemical/abl-bcr fusion protein, human
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1878-3686
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
496-506
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18538733-3' Untranslated Regions,
pubmed-meshheading:18538733-Animals,
pubmed-meshheading:18538733-Azacitidine,
pubmed-meshheading:18538733-Cell Line, Tumor,
pubmed-meshheading:18538733-Cell Proliferation,
pubmed-meshheading:18538733-Chromosomes, Human, Pair 14,
pubmed-meshheading:18538733-Chromosomes, Mammalian,
pubmed-meshheading:18538733-DNA Methylation,
pubmed-meshheading:18538733-DNA Modification Methylases,
pubmed-meshheading:18538733-Enzyme Inhibitors,
pubmed-meshheading:18538733-Fusion Proteins, bcr-abl,
pubmed-meshheading:18538733-Gene Expression Profiling,
pubmed-meshheading:18538733-Gene Expression Regulation, Leukemic,
pubmed-meshheading:18538733-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:18538733-Gene Silencing,
pubmed-meshheading:18538733-Humans,
pubmed-meshheading:18538733-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:18538733-Loss of Heterozygosity,
pubmed-meshheading:18538733-Lymphoma, T-Cell,
pubmed-meshheading:18538733-Lymphoproliferative Disorders,
pubmed-meshheading:18538733-Mice,
pubmed-meshheading:18538733-Mice, Inbred C57BL,
pubmed-meshheading:18538733-MicroRNAs,
pubmed-meshheading:18538733-Phenylbutyrates,
pubmed-meshheading:18538733-Philadelphia Chromosome,
pubmed-meshheading:18538733-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:18538733-Promoter Regions, Genetic,
pubmed-meshheading:18538733-Proto-Oncogene Proteins c-abl,
pubmed-meshheading:18538733-Time Factors,
pubmed-meshheading:18538733-Transfection,
pubmed-meshheading:18538733-Up-Regulation,
pubmed-meshheading:18538733-Whole-Body Irradiation
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pubmed:year |
2008
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pubmed:articleTitle |
Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression.
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pubmed:affiliation |
Cell Division and Cancer Group, Centro Nacional de Investigaciones Oncológicas (CNIO), E-28029 Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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