ArticleOncotarget2016
DDX3 enhances oncogenic KRAS‑induced tumor invasion in colorectal cancer via the β‑catenin/ZEB1 axis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.
- Prognostic value of ZEB-1 in solid tumors: a meta-analysis.BMC cancer · 2019Pooled it
- Prognostic significance of ZEB1 and ZEB2 in digestive cancers: a cohort-based analysis and secondary analysis.Oncotarget · 2017Pooled it
- Sex-linked helicases DDX3X and DDX3Y regulate G-quadruplex-associated stress in neurons.Cell death & disease · 2026Article
- Implication of Epigenetic Alterations of ZEB1 in Colorectal Cancer (CRC) Pathogenesis and Therapy Development.Current issues in molecular biology · 2026Review
- Targeting FAM134B-DDX3X axis inhibiting AKT signaling in hepatocellular carcinoma.Cell death & disease · 2025Article
- DDX3 participates in miRNA biogenesis and RNA interference through translational control of PACT and interaction with AGO2.FEBS open bio · 2025Article
- DEAD-box helicase family proteins: emerging targets in digestive system cancers and advances in targeted drug development.Journal of translational medicine · 2024Review
- Review
- Inhibition of SIRT7 overcomes sorafenib acquired resistance by suppressing ERK1/2 phosphorylation via the DDX3X-mediated NLRP3 inflammasome in hepatocellular carcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024Article
- DEAD-box RNA helicases with special reference to p68: Unwinding their biology, versatility, and therapeutic opportunity in cancer.Genes & diseases · 2023Review
- The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023Review
- KRAS Hijacks the miRNA Regulatory Pathway in Cancer.Cancer research · 2023Article
- Role and therapeutic potential of DEAD-box RNA helicase family in colorectal cancer.Frontiers in oncology · 2023Review
- DDX3 Upregulates Hydrogen Peroxide-Induced Melanogenesis in Sk-Mel-2 Human Melanoma Cells.Molecules (Basel, Switzerland) · 2022Article
- Disease-related protein co-expression networks are associated with the prognosis of resectable node-positive pancreatic ductal adenocarcinoma.Scientific reports · 2022Article
- DEAD-Box RNA Helicases DDX3X and DDX5 as Oncogenes or Oncosuppressors: A Network Perspective.Cancers · 2022Review
- DEAD/H-Box Helicases in Immunity, Inflammation, Cell Differentiation, and Cell Death and Disease.Cells · 2022Review
- DDX3 acts as a tumor suppressor in colorectal cancer as loss of DDX3 in advanced cancer promotes tumor progression by activating the MAPK pathway.International journal of biological sciences · 2022Article
- The DEAD-box protein family of RNA helicases: sentinels for a myriad of cellular functions with emerging roles in tumorigenesis.International journal of clinical oncology · 2021Review
- DDX3X: structure, physiologic functions and cancer.Molecular cancer · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DDX3 plays a dual role in colorectal cancer; however, the role and underlying mechanism of DDX3 in colorectal tumorigenesis remains unclear. Here, we provide evidence that DDX3 enhances oncogenic KRAS transcription via an increase in SP1 binding to its promoter. Accelerating oncogenic KRAS expression by DDX3 promotes the invasion capability via the ERK/PTEN/AKT/β-catenin cascade. Moreover, the β-catenin/ZEB1 axis is responsible for DDX3-induced cell invasiveness and xenograft lung tumor nodule formation. The xenograft lung tumor nodules induced by DDX3-overexpressing T84 stable clone were nearly suppressed by the inhibitor of AKT (perifosine) or β-catenin (XAV939). Among patients, high KRAS, positive nuclear β-catenin expression and high ZEB1 were more commonly occurred in high-DDX3 tumors than in low-DDX3 tumors. High-DDX3, high-KRAS, positive nuclear β-catenin tumors, and high-ZEB1 exhibited worse overall survival (OS) and relapse free survival (RFS) than their counterparts. In conclusion, DDX3 may play an oncogenic role to promote tumor growth and invasion in colon cancer cells via the β-catenin/ZEB1 axis due to increasing KRAS transcription. We therefore suggest that AKT or β-catenin may potentially act as a therapeutic target to improve tumor regression and outcomes in colorectal cancer patients who harbored high-DDX3 tumors.
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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.