Experiment Detail



Experiment IDEXP00261
ReferenceTitle: The IGF2 intronic miR-483 selectively enhances transcription from IGF2 fetalpromoters and enhances tumorigenesis.
Author: Liu M, Roth A, Yu M, Morris R, Bersani F, Rivera MN, Lu J, Shioda T, VasudevanS, Ramaswamy S, Maheswaran S, Diederichs S, Haber DA.
Journal: Genes Dev. 2013 Dec 1;27(23):2543-8. doi: 10.1101/gad.224170.113.
Abstract: Insulin-like growth factor 2 (IGF2), a developmentally regulated and maternallyimprinted gene, is frequently overexpressed in pediatric cancers. Although lossof imprinting (LOI) at fetal promoters contributes to increased IGF2 in tumors,the magnitude of IGF2 expression suggests the involvement of additionalregulatory mechanisms. A microRNA (miRNA) screen of primary Wilms' tumorsidentified specific overexpression of miR-483-5p, which is embedded within theIGF2 gene. Unexpectedly, the IGF2 mRNA itself is transcriptionally up-regulatedby miR-483-5p. A nuclear pool of miR-483-5p binds directly to the 5' untranslatedregion (UTR) of fetal IGF2 mRNA, enhancing the association of the RNA helicaseDHX9 to the IGF2 transcript and promoting IGF2 transcription. Ectopic expression of miR-483-5p in IGF2-dependent sarcoma cells is correlated with increasedtumorigenesis in vivo. Together, these observations suggest a functional positivefeedback loop of an intronic miRNA on transcription of its host gene.
PMID: 24298054
Expressiion ProfileDescription: microRNA Profiling in Wilms Tumors and Kidney Tissues
Organism: Homo sapiens
GEO ID: GSE50505
Platform: GPL17667
Number of samples: 28
Design and SampleCancer Type: kidney cancer
Cancer SubType: Wilms tumor
Cell Line: N/D
Experimental Design: cancer vs normal
Case Sample: Wilms tumor
Control Sample: normal kidney
Num of Case: 20
Num of Control: 3
Quantification Software: Limma
Num of miRNAs: 347
IdentificationNum of Up: 20
Num of Down: 42