ArticleCell death & disease2019
DDX17 promotes hepatocellular carcinoma progression via inhibiting Klf4 transcriptional activity.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- ZNF200 and DDX17 regulatory loop promotes tumor growth and metastasis by activating RBPJ transcription in non-small cell lung cancer.Science China. Life sciences · 2026Article
- TGF-β1/SMAD signaling downregulates KLF4 expression via direct transcriptional suppression and FAT10-mediated proteasomal degradation in hepatocellular carcinoma.Cell & bioscience · 2026Article
- Alternative splicing of KLF4 in myeloid cells: implications for cellular plasticity and trained immunity in cancer and inflammatory disease.Frontiers in immunology · 2025Review
- The advances of DEAD-box RNA helicase 17 in chronic non-infectious diseases.Frontiers in cardiovascular medicine · 2025Review
- DDX17-Mediated Upregulation of CXCL8 Promotes Hepatocellular Carcinoma ProgressionInternational journal of biological sciences · 2025Article
- DEAD-Box Helicase 17 exacerbates non-alcoholic steatohepatitis via transcriptional repression of cyp2c29, inducing hepatic lipid metabolism disorder and eliciting the activation of M1 macrophages.Clinical and translational medicine · 2024Article
- HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B.Cell reports. Medicine · 2023Article
- KRAS Hijacks the miRNA Regulatory Pathway in Cancer.Cancer research · 2023Article
- DEAD-Box Helicase 17 Promotes Amyloidogenesis by Regulating BACE1 Translation.Brain sciences · 2023Article
- LncRNA FAM225B Regulates PDIA4-Mediated Ovarian Cancer Cell Invasion and Migration via Modulating Transcription Factor DDX17.The breast journal · 2023Article
- DDX17 promotes the growth and metastasis of lung adenocarcinoma.Cell death discovery · 2022Article
- DDX55 promotes hepatocellular carcinoma progression by interacting with BRD4 and participating in exosome-mediated cell-cell communication.Cancer science · 2022Article
- Gastric Cancer Pre-Stage Detection and Early Diagnosis of Gastritis Using Serum Protein Signatures.Molecules (Basel, Switzerland) · 2022Article
- DUB3/KLF4 combats tumor growth and chemoresistance in hepatocellular carcinoma.Cell death discovery · 2022Article
- DDX56 transcriptionally activates MIST1 to facilitate tumorigenesis of HCC through PTEN-AKT signaling.Theranostics · 2022Article
- HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis.Frontiers in immunology · 2022Article
- DDX5 and DDX17-multifaceted proteins in the regulation of tumorigenesis and tumor progression.Frontiers in oncology · 2022Review
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- Identification of gene signatures and potential therapeutic targets for acquired chemotherapy resistance in gastric cancer patients.Journal of gastrointestinal oncology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DEAD box RNA helicase 17 (DDX17) is a transcriptional regulator of several transcription factors, which is more appreciated than its role in RNA metabolism. However, prognostic value and biofunction of DDX17 in HCC remain unclear. Illuminating the mechanism underlying the regulating HCC progression by DDX17 may contribute to therapeutic strategies. In our study, we report for the first time that DDX17 was overexpressed in HCC specimens by using The Cancer Genome Atlas (TCGA) and immunohistochemistry (IHC) and correlated to clinical pathological characteristics and patients' survival. In vitro, DDX17 was ascertained to alter HCC migratory and invasive capacities after overexpression and knockdown in HCC cell lines. Moreover, by performing co-immunoprecipitation (Co-IP) and GST-pull down assay, the physical association between DDX17 and Klf4 was discovered and validated. Additionally, DDX17 could modulate expressions of Klf4 target genes including E-cadherin, MMP2 by inhibiting the promoter activity. The potent correlation between DDX17 and Klf4 target gene expressions was further appraised by a same set of 30 HCC tissues. Besides, we discovered that DDX17 could not deploy its function in regulating Klf4 target gene expressions and HCC progression in Klf4-depletion condition. Intriguingly, DDX17 failed to interact with Klf4 once the zinc-finger domain was deleted and inhibited the binding of Klf4 on MMP-2 promoter. Collectively, our study enucleates novel mechanism of DDX17-mediated oncogenesis by suppressing the transcriptional activity of Klf4 thus is likely to be a therapeutic target in HCC.
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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.