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Publication : Accumulation of pre-let-7g and downregulation of mature let-7g with the depletion of EWS.

First Author  Sohn EJ Year  2012
Journal  Biochem Biophys Res Commun Volume  426
Issue  1 Pages  89-93
PubMed ID  22910415 Mgi Jnum  J:188129
Mgi Id  MGI:5439213 Doi  10.1016/j.bbrc.2012.08.041
Citation  Sohn EJ, et al. (2012) Accumulation of pre-let-7g and downregulation of mature let-7g with the depletion of EWS. Biochem Biophys Res Commun 426(1):89-93
abstractText  EWS functions in RNA splicing and transcription by encoding an RNA binding protein, which results in the chromosomal translocation t(11;22)(q24;q12) found in Ewing sarcoma. EWS interacts with the microprocessor complex involving Drosha and DGCR8, which play roles as the cofactors of primary microRNA processing. However, the role of EWS in microRNA biogenesis has not been investigated. Here, we show that endogenous EWS interacts with endogenous Drosha by IP-western blotting. In addition, EWS knockout mouse decreased the expression of Drosha. The depletion of EWS results in the accumulation of precursor let-7g but down-regulates mature let-7g in U2OS cells. Consistently, mature let 7g was suppressed in both Ewing sarcoma cell and primary Ewing sarcoma. Also, expression levels of Dicer and CCND1 (Cyclin D1), which are known target genes of the let-7 family were upregulated. Our findings suggest that EWS mediates generation of mature let-7g from pre-let-7g.
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