The DDX39B/FUT3/TGF?R-I axis promotes tumor metastasis and EMT in colorectal cancer

Abstract DDX39B is a member of the DEAD box (DDX) RNA helicase family required for nearly all cellular metabolic processes. The exact role and potential molecular mechanism in progression human colorectal cancer (CRC) remain to be investigated. In present study, we demonstrate that expression higher CRC tissues than adjacent normal tissues. Gain- loss-of-function assays revealed facilitates metastasis vivo vitro. Mechanistically, RNA-sequencing (RNA-seq) RNA-binding protein immunoprecipitation-sequencing (RIP-seq) showed binds directly FUT3 pre-mRNA upregulates expression. Splicing experiments vitro using Minigene assay confirmed promotes splicing. A nuclear cytoplasmic separation indicates enhances mRNA export FUT3. Upregulation accelerates fucosylation TGF?R-I, which activates TGF? signaling pathway eventually drives epithelial–mesenchymal transition (EMT) program contributes progression. These findings not only provide new insight into splicing as well tumorigenesis, but also shed light on effects aberrant