ArticleCell death discovery2025
CDK4/6-mediated phosphorylation of DUB3 promotes YAP1 stability and hepatocellular carcinoma progression.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed.
- Polyporusterone E, a Key Component ofInternational journal of molecular sciences · 2026Article
- Circulating miR-184 and miR-206 as predictive biomarkers for early recurrence in HBV-related hepatocellular carcinoma: a prospective study.BMC gastroenterology · 2026Article
- GPCRs as key regulators in wound healing.Frontiers in cell and developmental biology · 2026Review
- A Prognostic Risk Model for Hepatocellular Carcinoma Integrating Ferroptosis and Metabolic Reprogramming Signatures.Journal of Cancer · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most lethal malignancies, frequently characterized by high expression and activation of Yes-associated protein 1 (YAP1), a key effector in the Hippo signaling pathway. Despite its crucial role in HCC progression, effective therapies directly targeting YAP1 remain challenging, underscoring the need to explore the regulatory mechanisms underlying its aberrant expression and activation. In this study, we identify cyclin-dependent kinase 4 and 6 (CDK4/6) as uncharacterized regulators of YAP1 in HCC. Genetic ablation or pharmacological inhibition of CDK4/6 significantly destabilizes YAP1 and attenuates its oncogenic functions both in vitro and in vivo. Furthermore, we establish DUB3 as a bona fide deubiquitinase of YAP1. Mechanistically, CDK4/6 directly phosphorylates DUB3, enhancing its deubiquitinase activity towards YAP1, which promotes tumor growth and contributes to chemo-resistance in HCC. Collectively, our findings unveil the previously unrecognized function and significance of the CDK4/6-DUB3 axis in stabilizing YAP1 and provide a rationale for potential therapeutic interventions in the treatment of HCC.
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Registered trials
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