ArticleScientific reports2025
Blocking YAP1-Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous carcinoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
- Unraveling the molecular landscape: an overview on gene expression, epigenetic alterations, and therapeutic challenges in head and neck squamous cell carcinoma.Molecular genetics and genomics : MGG · 2026Review
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression.Clinical epigenetics · 2026Article
- Liriopesides B inhibits proliferation and metastasis and induces apoptosis of oral squamous cell carcinoma via the PI3K/Akt/mTOR signaling pathway.Translational cancer research · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Our research investigates the role of the YAP1-PPFIBP2 axis in the epithelial-mesenchymal transition (EMT) and its subsequent impact on invasion and migration in head and neck squamous cell carcinoma (HNSCC). Utilizing both in vitro assays and genomic analyses, we demonstrate that YAP1 upregulates EMT by suppressing PPFIBP2/liprin-β2 expression. This regulatory pathway contributes to enhanced invasiveness and correlates with poorer prognostic outcomes in HNSCC. We specifically knocked down YAP1 in SNU1041 and SCC9 cell lines using siRNA, resulting in reduced invasion and migration. These effects were reversed by subsequent administration of siPPFIBP2. In contrast, overexpression of YAP1 in SCC25 cells led to increased EMT marker activity and enhanced invasive behavior, supporting the functional role of this axis. Importantly, pharmacological inhibition of YAP1 using CA3 led to a notable decrease in EMT markers, invasion, and migration, suggesting that blocking the YAP1-PPFIBP2 axis may serve as an effective therapeutic strategy in HNSCC. In conclusion, our study identifies the YAP1-PPFIBP2 interaction as a crucial mediator of tumor aggressiveness in HNSCC, offering new insight into metastatic progression and highlighting a promising target for therapeutic intervention.
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Registered trials
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