ArticleCancers2025
PLS3 Is a Prognostic Biomarker and Correlates with Immune Infiltrates in Head and Neck Squamous Cell Carcinoma.
Article in Cancers, 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.
- Review
- Platelet transcriptomic signatures in pediatric brain tumors distinguish cancer from cancer-free control.Acta neuropathologica communications · 2026Article
- LONP2 Enhances Cervical Cancer Growth and Metastatic Potential by Upregulating PLS3 and Activating PI3K/AKT Signaling.Cancer management and research · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundHead and neck squamous cell carcinoma (HNSCC) features aggressive progression and a complex immunosuppressive microenvironment, contributing to poor patient prognosis and highlighting the need to identify key molecular drivers. The actin‑binding protein PLS3 (Plastin‑3) is involved in tumor metastasis, yet its expression, function, and therapeutic potential in HNSCC remain unclear.
methodsPLS3 expression was analyzed via polymerase chain reaction (PCR), Western blot (WB), and immunohistochemistry (IHC). PLS3 was knocked down in vitro to assess its effects on HNSCC cell functions, and in vivo models were established to evaluate tumor progression and immune microenvironment. Bioinformatics analyses explored the relationship between PLS3 and tumor immunity.
resultsPLS3 was upregulated in HNSCC tissues and correlated with adverse clinical outcomes. Knockdown of PLS3 inhibited cell proliferation, migration, and invasion in vitro, and suppressed tumor growth in vivo. Mechanistically, PLS3 promoted HNSCC progression by activating the epithelial-mesenchymal transition (EMT) program. Bioinformatics and animal studies further linked PLS3 overexpression to an immunosuppressive microenvironment characterized by reduced CD8+ T-cell infiltration and downregulated chemokine expression.
conclusionsThis study elucidates the oncogenic role of PLS3 in HNSCC and supports its potential as a prognostic biomarker and therapeutic target.
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