ArticleInternational journal of biological sciences2023
DBF4 Dependent Kinase Inhibition Suppresses Hepatocellular Carcinoma Progression and Potentiates Anti-Programmed Cell Death-1 Therapy.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Improving immunotherapy for the treatment of hepatocellular carcinoma: learning from patients and preclinical models.Gut and liver · 2025Review
- Clinical significance and pro-oncogenic function of DBF4 in clear cell renal cell carcinoma.BMC urology · 2025Article
- Prognostic and functional role of the nuclear export receptor 1 (XPO1) in gastrointestinal cancers: a potential novel target?Molecular biology reports · 2024Review
- Role and clinical value of serum hsa_tsr011468 in lung adenocarcinoma.Molecular medicine reports · 2024Article
- The prognostic significance and potential mechanism of DBF4 zinc finger in hepatocellular carcinoma.Scientific reports · 2024Article
- DHX37 Is a Promising Prognostic Biomarker and a Therapeutic Target for Immunotherapy and Chemotherapy in HCC.Cancers · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progression of hepatocellular carcinoma (HCC) remains a huge clinical challenge, and elucidation of the underlying molecular mechanisms is critical to develop effective therapeutic strategy. Dumbbell former 4 (DBF4) complexes with cell division cycle 7 (CDC7) to form DBF4-dependent kinase (DDK), playing instrumental roles in tumor cell survival, whereas its roles in HCC remain elusive. This study revealed that DBF4 expression was upregulated in HCC and constituted an independent prognostic factor of patient survival. We identified p65 as an upstream inducer which increased DBF4 expression by directly binding to its promoter. DBF4 accelerated HCC cell proliferation and tumorigenesis
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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.