pubmed-article:12878165 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C0035668 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C1519697 | lld:lifeskim |
pubmed-article:12878165 | lifeskim:mentions | umls-concept:C1519595 | lld:lifeskim |
pubmed-article:12878165 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:12878165 | pubmed:dateCreated | 2003-7-24 | lld:pubmed |
pubmed-article:12878165 | pubmed:abstractText | Activity of the independently regulated human c-myc P0 promoter has been associated with the undifferentiated status of leukemia cells as well as the hormone-independent proliferation of breast cancer cells. The P0 transcript is distinguished from the predominant P1 and P2 c-myc mRNAs by an approximately 639-nucleotide extension of the 5'-untranslated region. We hypothesized that this complex 5'-untranslated RNA sequence unique to the P0 transcript may contribute significantly to the composite regulation of the c-myc locus and that enforced intracellular synthesis of the isolated P0 5'-UTR, out of its native sequence context, might amplify or dominantly interfere with its normal regulatory function. Human tumor (HeLa) cells in which the isolated P0 5'-UTR was ectopically expressed displayed a dramatic decrease in anchorage-independent proliferation. Furthermore, P0 5'-UTR-expressing HeLa cells failed to form tumors when inoculated into SCID mice. This loss of tumorigenicity was associated with increases in levels of the c-Myc1 (p67) and c-Myc2 (p64) proteins and a 3- to 5-fold elevation of spontaneous apoptotic index. These results demonstrate that an isolated 5'-untranslated RNA sequence can be attributed potent in trans gene-regulatory and phenotype-altering capabilities and that extrinsic alterations in c-myc regulation can be utilized to reestablish the natural proapoptotic (tumor suppressor) activities associated with this protooncogene. | lld:pubmed |
pubmed-article:12878165 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:language | eng | lld:pubmed |
pubmed-article:12878165 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12878165 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12878165 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12878165 | pubmed:month | Aug | lld:pubmed |
pubmed-article:12878165 | pubmed:issn | 0014-4827 | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:GrizzleWillia... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:MillerDonald... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:EmanuelPeter... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:RuppertJ... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:BlumeScott... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:MengZhengZ | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:ShresthaKedar... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:SnyderRichard... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:StockardCecil... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:GuarcelloVinc... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:GartlandG... | lld:pubmed |
pubmed-article:12878165 | pubmed:author | pubmed-author:JonesDavid... | lld:pubmed |
pubmed-article:12878165 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12878165 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12878165 | pubmed:volume | 288 | lld:pubmed |
pubmed-article:12878165 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12878165 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12878165 | pubmed:pagination | 131-42 | lld:pubmed |
pubmed-article:12878165 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12878165 | pubmed:meshHeading | pubmed-meshheading:12878165... | lld:pubmed |
pubmed-article:12878165 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12878165 | pubmed:articleTitle | Inhibition of tumorigenicity by the 5'-untranslated RNA of the human c-myc P0 transcript. | lld:pubmed |
pubmed-article:12878165 | pubmed:affiliation | Department of Medicine, University of Alabama at Birmingham, Tumor Institute, Room 508, 1824 6th Avenue South, Birmingham, AL 35294-3300, USA. scott.blume@ccc.uab.edu | lld:pubmed |
pubmed-article:12878165 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12878165 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12878165 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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