ArticleCell death discovery2022
DDX39B contributes to the proliferation of colorectal cancer through direct binding to CDK6/CCND1.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- DDX39B drives the m6A modification of LDHA to promote trophoblast proliferation.Molecular genetics and genomics : MGG · 2026Article
- Article
- SNRPD2-mediated regulation of DDX39B splicing promotes endometrial cancer progression by suppressing the activation of CTSC cryptic exons.Cell death & disease · 2026Article
- CXCL12 deficiency promotes colorectal cancer progression and reduces anti-PD-L1 immunotherapy efficacy through MDSC regulation.Journal of translational medicine · 2025Article
- In vivo crosslinking and effective 2D enrichment for proteome wide interactome studies.Communications chemistry · 2025Article
- Sequence-Only Prediction of Super-Enhancers in Human Cell Lines Using Transformer Models.Biology · 2025Article
- Exploration of the Mechanism of Action ofJournal of hepatocellular carcinoma · 2025Article
- DEAD-box helicase family proteins: emerging targets in digestive system cancers and advances in targeted drug development.Journal of translational medicine · 2024Review
- Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression.Discover oncology · 2024Article
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
- Circular RNA in cancer.Nature reviews. Cancer · 2024Review
- Identification and Validation of Prognostic Model for Tumor Microenvironment-Associated Genes in Bladder Cancer Based on Single-Cell RNA Sequencing Data Sets.JCO precision oncology · 2024Article
- Critical Cellular Functions and Mechanisms of Action of the RNA Helicase UAP56.Journal of molecular biology · 2024Review
- Structural differences between the closely related RNA helicases, UAP56 and URH49, fashion distinct functional apo-complexes.Nature communications · 2024Article
- Network Pharmacological Analysis and Experimental Validation of the Effects of Silybin on Proliferation, Migration, and Immunotherapy of Papillary Thyroid Cancer.Endocrine, metabolic & immune disorders drug targets · 2024Article
- The Antitumor Effect of the DNA Polymerase Alpha Inhibitor ST1926 in Glioblastoma: A Proteomics Approach.International journal of molecular sciences · 2023Article
- Review
- Role and therapeutic potential of DEAD-box RNA helicase family in colorectal cancer.Frontiers in oncology · 2023Review
- Tumor Cell-Derived Exosomal circ-PRKCI Promotes Proliferation of Renal Cell Carcinoma via Regulating miR-545-3p/CCND1 Axis.Cancers · 2022Article
- mCells · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DDX39B (also called UAP56 or BAT1) which is a kind of DEAD-box family helicase plays pivotal roles in mRNA binding, splicing, and export. It has been found upregulated in many kinds of tumors as an oncogene. Nevertheless, the underlying molecular mechanisms of DDX39B in the proliferation of human colorectal cancer (CRC) remain fairly elusive. In our study, function experiments including the CCK8 and colony formation assay revealed that DDX39B facilitates CRC proliferation in vitro. DDX39B knockdown cells were administered for the orthotopic CRC tumor xenograft mouse model, after which tumor growth was monitored and immunohistochemistry (IHC) was performed to prove that DDX39B can also facilitates CRC proliferation in vivo. Flow cytometry demonstrated that DDX39B promotes the proliferation of CRC cells by driving the cell cycle from G0/G1 phase to the S phase. Mechanistically, RNA-binding protein immunoprecipitation-sequencing (RIP-seq) confirmed that DDX39B binds directly to the first exon of the CDK6/CCND1 pre-mRNA and upregulates their expression. Splicing experiments in vitro using a RT-PCR and gel electrophoresis assay confirmed that DDX39B promotes CDK6/CCND1 pre-mRNA splicing. Rescue experiments indicated that CDK6/CCND1 is a downstream effector of DDX39B-mediated CRC cell proliferation. Collectively, our results demonstrated that DDX39B and CDK6/CCND1 direct interactions serve as a CRC proliferation promoter, which can accelerate the G1/S phase transition to enhance CRC proliferation, and can offer novel and emerging treatment strategies targeting this cell proliferation-promoting gene.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.