ArticleCell death & disease2018
DDX39 promotes hepatocellular carcinoma growth and metastasis through activating Wnt/β-catenin pathway.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- Artificial Intelligence-Driven Construction of Predictive and Druggable Frameworks to an In Silico Bioengineering Evidence Support for Therapy of Esophageal Squamous Cell Carcinoma Patients: Insights from a Toll-like Receptor Signal with Th17 and T Helper Microenvironment.Bioengineering (Basel, Switzerland) · 2026Article
- SRSF3-TRIM28-MDC1 prevents DNA damage caused by R-loops in fatty liver disease in mice.JCI insight · 2026Article
- DExD-box helicase 39 A, targeted by coumestrol, facilitates the malignant behaviors of osteosarcoma cells.Hereditas · 2025Article
- SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.Oncogene · 2025Article
- DDX10 Exacerbates Exosomal PD-L1-Dependent T Cell Exhaustion via Phase Separation of Rab27b in Oral Squamous Cell Carcinoma.Research (Washington, D.C.) · 2025Article
- TRAIP enhances progression of tongue squamous cell carcinoma through EMT and Wnt/β-catenin signaling by interacting with DDX39A.BMC cancer · 2024Article
- Hub metastatic gene signature and risk score of breast cancer patients with small tumor sizes using WGCNA.Breast cancer (Tokyo, Japan) · 2024Article
- DDX RNA helicases: key players in cellular homeostasis and innate antiviral immunity.Journal of virology · 2024Review
- Structural differences between the closely related RNA helicases, UAP56 and URH49, fashion distinct functional apo-complexes.Nature communications · 2024Article
- Alternative splicing of IRF3 plays an important role in the development of hepatocarcinoma.Epigenetics · 2023Article
- DDX39B facilitates the malignant progression of hepatocellular carcinoma via activation of SREBP1-mediated de novo lipid synthesis.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Structural basis for high-order complex of SARNP and DDX39B to facilitate mRNP assembly.Cell reports · 2023Article
- DEAD-box RNA helicases with special reference to p68: Unwinding their biology, versatility, and therapeutic opportunity in cancer.Genes & diseases · 2023Review
- Construction of a Novel Diagnostic Model Based on Ferroptosis-Related Genes for Hepatocellular Carcinoma Using Machine and Deep Learning Methods.Journal of oncology · 2023Article
- The transcription factor TBP promotes hepatocellular carcinoma progression by activating AKT3.American journal of cancer research · 2023Article
- Stratifin Promotes Hepatocellular Carcinoma Progression by Modulating the Wnt/International journal of genomics · 2023Article
- Pathogenesis and Current Treatment Strategies of Hepatocellular Carcinoma.Biomedicines · 2022Review
- KCTD9 inhibits the Wnt/β-catenin pathway by decreasing the level of β-catenin in colorectal cancer.Cell death & disease · 2022Article
- DDX55 promotes hepatocellular carcinoma progression by interacting with BRD4 and participating in exosome-mediated cell-cell communication.Cancer science · 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
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the third leading cause of cancer related death worldwide; however, the molecular mechanisms regulating HCC progression remain largely unknown. In this study, we determined the role of DDX39 which a DEAD-box RNA helicase in HCC progression, and found DDX39 was upregulated in HCC tissues and cells, DDX39 expression was positive correlated with advanced clinical stage, survival analysis showed patients with high-DDX39 levels had poor outcome, it was an independent prognostic factor. Functional analysis revealed that DDX39 overexpression promoted HCC cell migration, invasion, growth, and metastasis, DDX39 knockdown inhibited HCC cell migration, invasion, growth, and metastasis. Mechanism analysis suggested DDX39 overexpression increased β-catenin expression in nucleus and increased Wnt/β-catenin pathway target genes levels, while DDX39 knockdown reduced this effect. Knockdown of Wnt/β-catenin pathway co-activators TCF4 and LEF1 in DDX39 overexpressing HCC cells inhibited Wnt/β-catenin pathway target genes. The invasion ability was also reduced, confirming DDX39 regulates HCC progression by activating Wnt/β-catenin pathway. In conclusion, we found DDX39 is a target and prognostic factor for HCC, and promotes HCC migration, invasion, growth, and metastasis by activating Wnt/β-catenin pathway.
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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.