ArticleCancer science2019
Oncogenic splicing abnormalities induced by DEAD-Box Helicase 56 amplification in colorectal cancer.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 57 citations in OpenAlex.
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- Novel driver gene FIRRM regulates the cell cycle for promoting tumor growth in hepatocellular carcinoma.Journal of gastroenterology · 2026Article
- SEC61G promotes colorectal cancer progression by regulating cytosolic CaJournal of gastroenterology · 2025Article
- Polarity Gene PARD6B Promotes Tumor Growth of Colorectal Cancer via Increasing MYC Expression.Cancer science · 2025Article
- Identifying the crucial oncogenic mechanisms of DDX56 based on a machine learning-based integration model of RNA-binding proteins.NPJ precision oncology · 2025Article
- SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.Oncogene · 2025Article
- Role of DEAD/DEAH-box helicases in immunity, infection and cancers.Cell communication and signaling : CCS · 2025Review
- DEAD-box helicase family proteins: emerging targets in digestive system cancers and advances in targeted drug development.Journal of translational medicine · 2024Review
- SpliceMutr Enables Pan-Cancer Analysis of Splicing-Derived Neoantigen Burden in Tumors.Cancer research communications · 2024Article
- Article
- Post-transcriptional regulation of DEAD-box RNA helicases in hematopoietic malignancies.Genes & diseases · 2024Review
- ATG10-dependent autophagy is required for DDX10 to regulate cell proliferation, apoptosis and stemness in colorectal cancer.Journal of cancer research and clinical oncology · 2024Article
- DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma.iScience · 2024Article
- Tumor suppressive role of the epigenetic master regulator BRD3 in colorectal cancer.Cancer science · 2024Article
- Spatial and single-cell colocalisation analysis reveals MDK-mediated immunosuppressive environment with regulatory T cells in colorectal carcinogenesis.EBioMedicine · 2024Article
- Transducin Beta-Like 2 is a Potential Driver Gene that Adapts to Endoplasmic Reticulum Stress to Promote Tumor Growth of Lung Adenocarcinoma.Annals of surgical oncology · 2023Article
- Role and therapeutic potential of DEAD-box RNA helicase family in colorectal cancer.Frontiers in oncology · 2023Review
- The splicing factor SF3B4 drives proliferation and invasion in cervical cancer by regulating SPAG5.Cell death discovery · 2022Article
- DEAD-box helicase 56 functions as an oncogene promote cell proliferation and invasion in gastric cancer via the FOXO1/p21 Cip1/c-Myc signaling pathway.Bioengineered · 2022Article
- RNA-interference screen for p53 regulators unveils a role of WDR75 in ribosome biogenesis.Cell death and differentiation · 2022Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative splicing, regulated by DEAD-Box Helicase (DDX) families, plays an important role in cancer. However, the relationship between the DDX family and cancer has not been fully elucidated. In the present study, we identified a candidate oncogene DDX56 on Ch.7p by a bioinformatics approach using The Cancer Genome Atlas (TCGA) dataset of colorectal cancer (CRC). DDX56 expression was measured by RT-qPCR and immunochemical staining in 108 CRC patients. Clinicopathological and survival analyses were carried out using three CRC datasets. Biological roles of DDX56 were explored by gene set enrichment analysis (GSEA), and cell proliferation in vitro and in vivo, cell cycle assays, and using DDX56-knockdown or overexpressed CRC cells. RNA sequencing was carried out to elucidate the effect of DDX56 on mRNA splicing. We found that DDX56 expression was positively correlated with the amplification of DDX56 and was upregulated in CRC cells. High DDX56 expression was associated with lymphatic invasion and distant metastasis and was an independent poor prognostic factor. In vitro analysis, in vivo analysis and GSEA showed that DDX56 promoted proliferation ability through regulating the cell cycle. DDX56 knockdown reduced intron retention and tumor suppressor WEE1 expression, which functions as a G2-M DNA damage checkpoint. We have identified DDX56 as a novel oncogene and prognostic biomarker of CRC that promotes alternative splicing of WEE1.
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