Linked Life Data

20099276

Source:http://linkedlifedata.com/resource/pubmed/id/20099276

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pubmed-article:20099276pubmed:abstractTextCancer cells that develop resistance to chemotherapeutic agents are a major clinical obstacle in the successful treatment of breast cancer. Acquired cancer chemoresistance is a multifactorial phenomenon, involving various mechanisms and processes. Recent studies suggest that chemoresistance may be linked to drug-induced dysregulation of microRNA function. Furthermore, mounting evidence indicates the existence of similarities between drug-resistant and metastatic cancer cells in terms of resistance to apoptosis and enhanced invasiveness. We studied the role of miRNA alterations in the acquisition of cisplatin-resistant phenotype in MCF-7 human breast adenocarcinoma cells. We identified a total of 103 miRNAs that were overexpressed or underexpressed (46 upregulated and 57 downregulated) in MCF-7 cells resistant to cisplatin. These differentially expressed miRNAs are involved in the control of cell signaling, cell survival, DNA methylation and invasiveness. The most significantly dysregulated miRNAs were miR-146a, miR-10a, miR-221/222, miR-345, miR-200b and miR-200c. Furthermore, we demonstrated that miR-345 and miR-7 target the human multidrug resistance-associated protein 1. These results suggest that dysregulated miRNA expression may underlie the abnormal functioning of critical cellular processes associated with the cisplatin-resistant phenotype.lld:pubmed
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pubmed-article:20099276pubmed:articleTitleAlterations of microRNAs and their targets are associated with acquired resistance of MCF-7 breast cancer cells to cisplatin.lld:pubmed
pubmed-article:20099276pubmed:affiliationDivision of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA. igor.pogribny@fda.hhs.govlld:pubmed
pubmed-article:20099276pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20099276pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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