MiR-15a and miR-16-1 cluster functions in human leukemia Export

@article{citeulike:2626393, abstract = {MicroRNAs (miRNAs) are short noncoding RNAs regulating gene expression that play roles in human diseases, including cancer. Each miRNA is predicted to regulate hundreds of transcripts, but only few have experimental validation. In chronic lymphocytic leukemia (CLL), the most common adult human leukemia, miR-15a and miR-16-1 are lost or down-regulated in the majority of cases. After our previous work indicating a tumor suppressor function of miR-15a/16-1 by targeting the BCL2 oncogene, here, we produced a high-throughput profiling of genes modulated by miR-15a/16-1 in a leukemic cell line model (MEG-01) and in primary CLL samples. By combining experimental and bioinformatics data, we identified a miR-15a/16-1-gene signature in leukemic cells. Among the components of the miR-15a/16-1 signature, we observed a statistically significant enrichment in AU-rich elements (AREs). By examining the Gene Ontology (GO) database, a significant enrichment in cancer genes (such as MCL1, BCL2, ETS1, or JUN) that directly or indirectly affect apoptosis and cell cycle was found. 10.1073/pnas.0800121105}, author = {Calin, George A. and Cimmino, Amelia and Fabbri, Muller and Ferracin, Manuela and Wojcik, Sylwia E. and Shimizu, Masayoshi and Taccioli, Cristian and Zanesi, Nicola and Garzon, Ramiro and Aqeilan, Rami I. and Alder, Hansjuerg and Volinia, Stefano and Rassenti, Laura and Liu, Xiuping and Liu, Chang-Gong and Kipps, Thomas J. and Negrini, Massimo and Croce, Carlo M.}, citeulike-article-id = {2626393}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0800121105}, citeulike-linkout-1 = {http://www.pnas.org/cgi/content/abstract/105/13/5166}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/18362358}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=18362358}, day = {1}, doi = {10.1073/pnas.0800121105}, journal = {Proceedings of the National Academy of Sciences}, keywords = {cancer, clustering, functional\_annotation, human, microrna, target}, month = {April}, number = {13}, pages = {5166--5171}, posted-at = {2008-04-03 16:12:54}, priority = {0}, title = {MiR-15a and miR-16-1 cluster functions in human leukemia}, url = {http://dx.doi.org/10.1073/pnas.0800121105}, volume = {105}, year = {2008} }

TY - JOUR ID - citeulike:2626393 L3 - citeulike-article-id:2626393 N2 - MicroRNAs (miRNAs) are short noncoding RNAs regulating gene expression that play roles in human diseases, including cancer. Each miRNA is predicted to regulate hundreds of transcripts, but only few have experimental validation. In chronic lymphocytic leukemia (CLL), the most common adult human leukemia, miR-15a and miR-16-1 are lost or down-regulated in the majority of cases. After our previous work indicating a tumor suppressor function of miR-15a/16-1 by targeting the BCL2 oncogene, here, we produced a high-throughput profiling of genes modulated by miR-15a/16-1 in a leukemic cell line model (MEG-01) and in primary CLL samples. By combining experimental and bioinformatics data, we identified a miR-15a/16-1-gene signature in leukemic cells. Among the components of the miR-15a/16-1 signature, we observed a statistically significant enrichment in AU-rich elements (AREs). By examining the Gene Ontology (GO) database, a significant enrichment in cancer genes (such as MCL1, BCL2, ETS1, or JUN) that directly or indirectly affect apoptosis and cell cycle was found. 10.1073/pnas.0800121105 IS - 13 JF - Proceedings of the National Academy of Sciences EP - 5171 TI - MiR-15a and miR-16-1 cluster functions in human leukemia VL - 105 SP - 5166 KW - cancer KW - clustering KW - functional_annotation KW - human KW - microrna KW - target AU - Calin, George AU - Cimmino, Amelia AU - Fabbri, Muller AU - Ferracin, Manuela AU - Wojcik, Sylwia AU - Shimizu, Masayoshi AU - Taccioli, Cristian AU - Zanesi, Nicola AU - Garzon, Ramiro AU - Aqeilan, Rami AU - Alder, Hansjuerg AU - Volinia, Stefano AU - Rassenti, Laura AU - Liu, Xiuping AU - Liu, Chang-Gong AU - Kipps, Thomas AU - Negrini, Massimo AU - Croce, Carlo PY - 2008/04/01/ UR - http://dx.doi.org/10.1073/pnas.0800121105 ER -