ArticleScientific reports2025
Loss of Sirtuin 7 impairs cell motility and proliferation and enhances S-phase cell arrest after 5-fluorouracil treatment in head and neck cancer.
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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Who cites it
4 citing papers in PubMed.
- Development and Characterization of a Guar Gum Bionanocomposite Loaded with Biogenic Selenium Nanoparticles and Its Cytotoxic Evaluation.Gels (Basel, Switzerland) · 2026Article
- A Double-Edged Role for SIRT7 in Cancer: Can Anti-Cancer Immunity Tip the Balance?Pharmaceuticals (Basel, Switzerland) · 2025Review
- Sirtuins and tumor immunity: mechanistic insights, immunotherapy prospects, and therapeutic horizons.Frontiers in immunology · 2025Review
- Organoid Technology in Precision Medicine for Head and Neck Cancer.Oncology research · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
Sirtuin 7 (SIRT7), a member of the sirtuin family of NAD+-dependent deacetylases, plays a vital role in cancer, exhibiting context-dependent functions across various malignancies. Our study investigates the role of SIRT7 depletion in head and neck squamous cell carcinoma (HNSCC) progression. In vitro and 3D organotypic models demonstrated that SIRT7 knock-out attenuates cancer cell viability, proliferation, and motility as well as induces downregulation of migration- and epithelial-mesenchymal transition (EMT)-related gene expression. Moreover, the SIRT7 loss results in slower organoid formation and less invasive organoid morphology, validated by vimentin downregulation. The SIRT7 loss potentiates S-phase arrest in cell cycle progression after 5-FU treatment and elevates the ratio of dead cells. Additionally, SIRT7 deletion reduces the expression of G1 phase-associated proteins, Cyclin D and CDK4. Altogether, our study highlights SIRT7 as a promising therapeutic target in HNSCC, enhancing the effectiveness of treatment modalities such as combinational treatment.
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