XRN2 promotes EMT and metastasis through regulating maturation of miR-10a. Oncogene 2017 Jul 06;36(27):3925-3933
Date
03/21/2017Pubmed ID
28319071DOI
10.1038/onc.2017.39Scopus ID
2-s2.0-85015661507 (requires institutional sign-in at Scopus site) 23 CitationsAbstract
MicroRNAs (miRNAs) have been proposed as critical regulatory molecules in the epithelial-mesenchymal transition (EMT) program. However, the roles of mature miRNA biogenesis during EMT process needs to be defined. Here we determined that increased expression of XRN2 induced EMT and promoted metastasis in vitro and in vivo. Furthermore, we uncovered that XRN2 functions as pro-metastatic gene, which accelerates miR-10a maturation by binding pre-miR-10a in a DICER-independent manner. These findings suggest that XRN2 is a novel regulator of EMT that contributes to the metastatic processes in lung cancer through a novel miRNA regulatory mechanism.
Author List
Zhang H, Lu Y, Chen E, Li X, Lv B, Vikis HG, Liu PMESH terms used to index this publication - Major topics in bold
AnimalsCarcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Cell Movement
DEAD-box RNA Helicases
Disease-Free Survival
Epithelial-Mesenchymal Transition
Exoribonucleases
Female
Gene Expression Regulation, Neoplastic
Humans
Kaplan-Meier Estimate
Lung Neoplasms
Mice, Inbred NOD
Mice, SCID
MicroRNAs
Neoplasm Transplantation
Prognosis
Proportional Hazards Models
Protein Binding
RNA Processing, Post-Transcriptional
Ribonuclease III
