Widespread microRNA repression by Myc contributes to tumorigenesis.

@article{citeulike:2105952, abstract = {The c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies. Myc is known to directly upregulate a pro-tumorigenic group of microRNAs (miRNAs) known as the miR-17-92 cluster. Through the analysis of human and mouse models of B cell lymphoma, we show here that Myc regulates a much broader set of miRNAs than previously anticipated. Unexpectedly, the predominant consequence of activation of Myc is widespread repression of miRNA expression. Chromatin immunoprecipitation reveals that much of this repression is likely to be a direct result of Myc binding to miRNA promoters. We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis.}, address = {[1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. [2] These authors contributed equally to this work.}, author = {Chang, Tsung-Cheng C. and Yu, Duonan and Lee, Yun-Sil S. and Wentzel, Erik A. A. and Arking, Dan E. E. and West, Kristin M. M. and Dang, Chi V. V. and Thomas-Tikhonenko, Andrei and Mendell, Joshua T. T. }, citeulike-article-id = {2105952}, doi = {http://dx.doi.org/10.1038/ng.2007.30}, issn = {1546-1718}, journal = {Nature Genetics}, keywords = {cancer, microrna, myc}, month = {December}, number = {1}, pages = {43--50}, posted-at = {2008-01-16 09:40:45}, priority = {0}, title = {Widespread microRNA repression by Myc contributes to tumorigenesis.}, url = {http://dx.doi.org/10.1038/ng.2007.30}, volume = {40}, year = {2007} }

TY - JOUR ID - citeulike:2105952 L3 - citeulike-article-id:2105952 TI - Widespread microRNA repression by Myc contributes to tumorigenesis. JF - Nature Genetics VL - 40 IS - 1 SP - 43 EP - 50 AD - [1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. [2] These authors contributed equally to this work. SN - 1546-1718 N2 - The c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies. Myc is known to directly upregulate a pro-tumorigenic group of microRNAs (miRNAs) known as the miR-17-92 cluster. Through the analysis of human and mouse models of B cell lymphoma, we show here that Myc regulates a much broader set of miRNAs than previously anticipated. Unexpectedly, the predominant consequence of activation of Myc is widespread repression of miRNA expression. Chromatin immunoprecipitation reveals that much of this repression is likely to be a direct result of Myc binding to miRNA promoters. We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis. KW - cancer KW - microrna KW - myc AU - Chang, Tsung-Cheng AU - Yu, Duonan AU - Lee, Yun-Sil AU - Wentzel, Erik AU - Arking, Dan AU - West, Kristin AU - Dang, Chi AU - Thomas-Tikhonenko, Andrei AU - Mendell, Joshua PY - 2007/12/09/ UR - http://dx.doi.org/10.1038/ng.2007.30 ER -