| Literature DB >> 27210763 |
Hanane Ennajdaoui1, Jonathan M Howard2, Timothy Sterne-Weiler1, Fereshteh Jahanbani3, Doyle J Coyne2, Philip J Uren4, Marija Dargyte2, Sol Katzman5, Jolene M Draper2, Andrew Wallace2, Oscar Cazarez2, Suzanne C Burns6, Mei Qiao6, Lindsay Hinck2, Andrew D Smith4, Masoud M Toloue7, Benjamin J Blencowe8, Luiz O F Penalva6, Jeremy R Sanford9.
Abstract
Insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) expression correlates with malignancy, but its role(s) in pathogenesis remains enigmatic. We interrogated the IGF2BP3-RNA interaction network in pancreatic ductal adenocarcinoma (PDAC) cells. Using a combination of genome-wide approaches, we have identified 164 direct mRNA targets of IGF2BP3. These transcripts encode proteins enriched for functions such as cell migration, proliferation, and adhesion. Loss of IGF2BP3 reduced PDAC cell invasiveness and remodeled focal adhesion junctions. Individual nucleotide resolution crosslinking immunoprecipitation (iCLIP) revealed significant overlap of IGF2BP3 and microRNA (miRNA) binding sites. IGF2BP3 promotes association of the RNA-induced silencing complex (RISC) with specific transcripts. Our results show that IGF2BP3 influences a malignancy-associated RNA regulon by modulating miRNA-mRNA interactions.Entities:
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Year: 2016 PMID： 27210763 PMCID： PMC4889463 DOI： 10.1016/j.celrep.2016.04.083
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423