| pubmed-article:19270061 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C1332002 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:19270061 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:19270061 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:19270061 | pubmed:dateCreated | 2009-5-22 | lld:pubmed |
| pubmed-article:19270061 | pubmed:abstractText | Breast cancer resistance protein (BCRP/ABCG2) is a molecular determinant of pharmacokinetic properties of many drugs in humans. To understand post-transcriptional regulation of ABCG2 and the role of microRNAs (miRNAs) in drug disposition, we found that microRNA-328 (miR-328) might readily target the 3'-untranslated region (3'-UTR) of ABCG2 when considering target-site accessibility. We then noted 1) an inverse relation between the levels of miR-328 and ABCG2 in MCF-7 and MCF-7/MX100 breast cancer cells and 2) that miR-328 levels could be rescued in MCF-7/MX100 cells by transfection with miR-328 plasmid. Luciferase reporter assays showed that ABCG2 3'-UTR-luciferase activity was decreased more than 50% in MCF-7/MX100 cells after transfection with miR-328 plasmid, the activity was increased over 100% in MCF-7 cells transfected with a miR-328 antagomir, and disruption of miR-328 response element within ABCG2 3'-UTR led to a 3-fold increase in luciferase activity. Furthermore, the level of ABCG2 protein was down-regulated when miR-328 was over-expressed, and the level was up-regulated when miR-328 was inhibited by selective antagomir. Altered ABCG2 protein expression was associated with significantly declined or elevated levels of ABCG2 3'-UTR and coding sequence mRNAs, suggesting possible involvement of the mechanism of mRNA cleavage. Finally, miR-328-directed down-regulation of ABCG2 expression in MCF-7/MX100 cells resulted in an increased mitoxantrone sensitivity, as manifested by a significantly lower IC(50) value (2.46 +/- 1.64 microM) compared with the control (151 +/- 32 microM). Together, these findings suggest that miR-328 targets ABCG2 3'-UTR and, consequently, controls ABCG2 protein expression and influences drug disposition in human breast cancer cells. | lld:pubmed |
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| pubmed-article:19270061 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19270061 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19270061 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19270061 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19270061 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19270061 | pubmed:issn | 1521-0111 | lld:pubmed |
| pubmed-article:19270061 | pubmed:author | pubmed-author:MorrisMarilyn... | lld:pubmed |
| pubmed-article:19270061 | pubmed:author | pubmed-author:YuAi-MingAM | lld:pubmed |
| pubmed-article:19270061 | pubmed:author | pubmed-author:PanYu-ZhuoYZ | lld:pubmed |
| pubmed-article:19270061 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19270061 | pubmed:volume | 75 | lld:pubmed |
| pubmed-article:19270061 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19270061 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19270061 | pubmed:pagination | 1374-9 | lld:pubmed |
| pubmed-article:19270061 | pubmed:dateRevised | 2010-9-22 | lld:pubmed |
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| pubmed-article:19270061 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19270061 | pubmed:articleTitle | MicroRNA-328 negatively regulates the expression of breast cancer resistance protein (BCRP/ABCG2) in human cancer cells. | lld:pubmed |
| pubmed-article:19270061 | pubmed:affiliation | Department of Pharmaceutical Sciences, University at Buffalo, The State University of New York, NY 14260-1200, USA. | lld:pubmed |
| pubmed-article:19270061 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19270061 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19270061 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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