ArticleMolecular oncology2021
The RNA-helicase DDX21 upregulates CEP55 expression and promotes neuroblastoma.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- DDX21 Promotes Breast Cancer Growth and Metastasis via Stimulating RNAPII Elongation During Hypoxia.MedComm · 2026Article
- Ubiquitination of DDX21 by HERC2 induces a dormancy-like phenotype via the NUCKS1-p21/p27 axis to promote radio-resistance in colorectal cancer cells.Cell death & disease · 2026Article
- Identification of Crucial Genes Associated With MYCN-Driven Neuroblastoma Based on Single-Cell Analysis and Machine Learning.Cancer medicine · 2025Article
- Competitive binding between DDX21 and SIRT7 enhances NAT10-mediated acCell death & disease · 2025Article
- The liver-specific long noncoding RNA FAM99B inhibits ribosome biogenesis and cancer progression through cleavage of dead-box Helicase 21.Cell death & disease · 2025Article
- DDX21 Is a Potential Biomarker for Predicting Recurrence and Prognosis in Hepatocellular Carcinoma.Analytical cellular pathology (Amsterdam) · 2025Article
- DDX21 at the Nexus of RNA Metabolism, Cancer Oncogenesis, and Host-Virus Crosstalk: Decoding Its Biomarker Potential and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Article
- CEP55 predicts the poor prognosis and promotes tumorigenesis in endometrial cancer by regulating the Foxo1 signaling.Molecular and cellular biochemistry · 2023Article
- MiRNA and Potential Prognostic Value in Non-Smoking Females with Lung Adenocarcinoma by High-Throughput Sequencing.International journal of general medicine · 2023Article
- CEP55 as a promising biomarker and therapeutic target on gallbladder cancer.Frontiers in oncology · 2023Article
- DDX55 promotes hepatocellular carcinoma progression by interacting with BRD4 and participating in exosome-mediated cell-cell communication.Cancer science · 2022Article
- DDX21 Interacts with WDR5 to Promote Colorectal Cancer Cell Proliferation by Activating CDK1 Expression.Journal of Cancer · 2022Article
- Nanotechnology-Based Diagnostic and Therapeutic Strategies for Neuroblastoma.Frontiers in pharmacology · 2022Review
- Pan-cancer analysis reveals DDX21 as a potential biomarker for the prognosis of multiple tumor types.Frontiers in oncology · 2022Article
- Synthetic lethal interactions of DEAD/H-box helicases as targets for cancer therapy.Frontiers in oncology · 2022Review
- Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 25% of human neuroblastoma is caused by amplification of the MYCN oncogene, which leads to overexpression of N-Myc oncoprotein. The survival rate for this patient subtype is <50%. Here, we show that N-Myc protein bound to the DEAD-box RNA helicase DDX21 gene promoter and upregulated DDX21 mRNA and protein expression. Genome-wide differential gene expression studies identified centrosomal protein CEP55 as one of the genes most dramatically downregulated after DDX21 knockdown in MYCN-amplified neuroblastoma cells. Knocking down DDX21 or CEP55 reduced neuroblastoma cell cytoskeleton stability and cell proliferation and all but abolished clonogenic capacity. Importantly, DDX21 knockdown initially induced tumor regression in neuroblastoma-bearing mice and suppressed tumor progression. In human neuroblastoma tissues, a high level of DDX21 expression correlated with a high level of N-Myc expression and with CEP55 expression, and independently predicted poor patient prognosis. Taken together, our data show that DDX21 induces CEP55 expression, MYCN-amplified neuroblastoma cell proliferation, and tumorigenesis, and that DDX21 and CEP55 are valid therapeutic targets for the treatment of MYCN-amplified neuroblastoma.
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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 OpenQuestion graph.