ArticleCell death & disease2021
The DDX39B/FUT3/TGFβR-I axis promotes tumor metastasis and EMT in colorectal cancer.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Genome-wide association studies in a large Korean cohort identify quantitative trait loci for 36 traits and illuminate their genetic architectures.Nature communications · 2025Pooled it
- CMS4 epithelial-intrinsic glycosyltransferase GALNT5 promotes tumor aggressiveness and correlates with poor survival in colorectal cancer.Scientific reports · 2026Article
- Transcriptome Analysis of TGFBI Knockdown vs Normal Corneal Epithelial Cells: Implications for TGFBI Corneal Dystrophy Treatment.Biochemical genetics · 2026Article
- Utilizing clinical features, genetic mutations, and a 14-gene molecular assay for optimizing the management of multiple primary lung cancer.Translational lung cancer research · 2026Article
- L-Fucose: a dietary sugar with multifaceted potential in the biology and therapy of cancer.Nature reviews. Cancer · 2026Review
- SNRPD2-mediated regulation of DDX39B splicing promotes endometrial cancer progression by suppressing the activation of CTSC cryptic exons.Cell death & disease · 2026Article
- Fucose metabolism as a central axis linking inflammation, immunity, and cancer in the gut.Frontiers in immunology · 2026Review
- FUT3 mediated GRP78 fucosylation promotes colorectal cancer survival and proliferation under glucose restriction via PERK/ATF4/STC2 axis.NPJ precision oncology · 2025Article
- FUT3-B3GNT3 interaction promotes pancreatic cancer progression and chemoresistance via NF-κB signaling mediated autophagy.European journal of medical research · 2025Article
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- CXCL12 deficiency promotes colorectal cancer progression and reduces anti-PD-L1 immunotherapy efficacy through MDSC regulation.Journal of translational medicine · 2025Article
- DEAD/H-box RNA helicase 10 promotes pancreatic cancer cell proliferationWorld journal of gastrointestinal oncology · 2025Article
- Article
- Proteomic characterization of MET-amplified esophageal adenocarcinomas reveals enrichment of alternative splicing- and androgen signaling-related proteins.Cellular and molecular life sciences : CMLS · 2025Article
- Potential therapeutic targets for colorectal cancer and its subsites: evidence from the proteome-wide Mendelian randomization analyses.Translational cancer research · 2025Article
- The role of glycan-lectin interactions in the tumor microenvironment: immunosuppression regulators of colorectal cancer.American journal of cancer research · 2025Review
- DDX10 Exacerbates Exosomal PD-L1-Dependent T Cell Exhaustion via Phase Separation of Rab27b in Oral Squamous Cell Carcinoma.Research (Washington, D.C.) · 2025Article
- DEAD-box helicase family proteins: emerging targets in digestive system cancers and advances in targeted drug development.Journal of translational medicine · 2024Review
- RFW captures species-level metagenomic functions by integrating genome annotation information.Cell reports methods · 2024Article
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DDX39B is a member of the DEAD box (DDX) RNA helicase family required for nearly all cellular RNA metabolic processes. The exact role and potential molecular mechanism of DDX39B in the progression of human colorectal cancer (CRC) remain to be investigated. In the present study, we demonstrate that DDX39B expression is higher in CRC tissues than in adjacent normal tissues. Gain- and loss-of-function assays revealed that DDX39B facilitates CRC metastasis in vivo and in vitro. Mechanistically, RNA-sequencing (RNA-seq) and RNA-binding protein immunoprecipitation-sequencing (RIP-seq) showed that DDX39B binds directly to the FUT3 pre-mRNA and upregulates FUT3 expression. Splicing experiments in vitro using a Minigene assay confirmed that DDX39B promotes FUT3 pre-mRNA splicing. A nuclear and cytoplasmic RNA separation assay indicates that DDX39B enhances the mRNA export of FUT3. Upregulation of FUT3 accelerates the fucosylation of TGFβR-I, which activates the TGFβ signaling pathway and eventually drives the epithelial-mesenchymal transition (EMT) program and contributes to CRC progression. These findings not only provide new insight into the role of DDX39B in mRNA splicing and export as well as in tumorigenesis, but also shed light on the effects of aberrant fucosylation on CRC progression.
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