ArticleInternational journal of biological sciences2025
DDX17-Mediated Upregulation of CXCL8 Promotes Hepatocellular Carcinoma Progression
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
3 citing papers in PubMed.
- DDX17-mediated raptor-dependent mTORC1 activation links autophagy inhibition and metabolic compensation in HCC development.Cellular & molecular biology letters · 2026Article
- [Silencing DDX17 inhibits proliferation and migration of pulmonary arterial smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Role of DEAD/DEAH-box helicases in immunity, infection and cancers.Cell communication and signaling : CCS · 2025Review
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a well-known inflammation-related cancer, that accounts for fifth most prevalent neoplasm and the third major driver of cancer associated fatality globally. Accumulating evidence has elucidated that C-X-C motif chemokine ligands (CXCLs) are aberrantly upregulated in HCC and are involved in inflammation-induced hepatocarcinogenesis and metastasis. Herein, we identified a novel function of DEAD-box RNA helicase 17 (DDX17) as an oncogenic factor via transactivating CXCL8 in HCC. Unlike the adjacent nontumor tissues, DDX17 was highly expressed in tumor tissues compared in two independent cohorts and that it acts as an independent prognostic indicator for patients who have HCC. Mechanistically, DDX17 interacts with β-catenin and NF-κB, and promotes their nuclear translocation to promote the transcription of the inflammatory gene CXCL8, thus promoting HCC proliferation and invasion
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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 Socratic graph.