ArticleBritish journal of cancer2019
Synergistic antitumour activity of HDAC inhibitor SAHA and EGFR inhibitor gefitinib in head and neck cancer: a key role for ΔNp63α.
Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Genetic susceptibility, risk prediction, and druggable targets for oropharyngeal cancer: a UK Biobank study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- Head and neck squamous cell carcinoma: current and emerging therapeutic strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
- NSD2 upregulation is driven by high-risk HPV E6/E7 and disrupts epithelial differentiation in HPV-associated head and neck cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Phytochemicals as Emerging Antiproliferative Agents in Head and Neck Cancer: Molecular Mechanisms and Therapeutic Strategies.Pharmacology · 2026Review
- Molecular Crosstalk and Therapeutic Synergy: Tyrosine Kinase Inhibitors and Cannabidiol in Oral Cancer Treatment.Current issues in molecular biology · 2025Review
- Acquired vulnerability against EGF receptor inhibition in gastric cancer promoted by class I histone deacetylase inhibitor entinostat.Neoplasia (New York, N.Y.) · 2025Article
- Advances in the study of posttranslational modifications of histones in head and neck squamous cell carcinoma.Clinical epigenetics · 2024Review
- Complex and variable regulation of ΔNp63 and TAp63 by TGFβ has implications for the dynamics of squamous cell epithelial to mesenchymal transition.Scientific reports · 2024Article
- Enabling Single-Cell Drug Response Annotations from Bulk RNA-Seq Using SCAD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- An integrative approach toward identification and analysis of therapeutic targets involved in HPV pathogenesis with a focus on carcinomas.Cancer biomarkers : section A of Disease markers · 2023Article
- An ErbB Lineage Co-Regulon Harbors Potentially Co-Druggable Targets for Multimodal Precision Therapy in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2022Article
- Emerging tyrosine kinase inhibitors for head and neck cancer.Expert opinion on emerging drugs · 2022Review
- A toolbox for class I HDACs reveals isoform specific roles in gene regulation and protein acetylation.PLoS genetics · 2022Article
- Regulation of epithelial-mesenchymal transition by protein lysine acetylation.Cell communication and signaling : CCS · 2022Review
- High Risk-Human Papillomavirus in HNSCC: Present and Future Challenges for Epigenetic Therapies.International journal of molecular sciences · 2022Review
- Identifying pathways regulating the oncogenic p53 family member ΔNp63 provides therapeutic avenues for squamous cell carcinoma.Cellular & molecular biology letters · 2022Article
- HPV-mediated regulation of SMAD4 modulates the DNA damage response in head and neck cancer.Journal of experimental & clinical cancer research : CR · 2022Article
- The UBC9/SUMO pathway affects E-cadherin cleavage in HPV-positive head and neck cancer.Frontiers in molecular biosciences · 2022Article
- Suberoylanilide Hydroxamic Acid (SAHA) Treatment Reveals Crosstalk Among Proteome, Phosphoproteome, and Acetylome in Nasopharyngeal Carcinoma Cells.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpidermal growth factor receptor (EGFR) overexpression is associated with the development of head and neck cancer (HNC) and represents one of the main therapeutic targets for this disease. The use of EGFR inhibitors has limited efficacy due to their primary and acquired resistance, partially because of increased epithelial to mesenchymal transition (EMT). The HDAC inhibitor SAHA has been shown to revert EMT in different tumours, including HNC. In this study, we investigated the cooperative role of SAHA and the EGFR tyrosine kinase inhibitor gefitinib in both HPV-positive and HPV-negative HNC cell lines.
methodsA panel of 12 HPV-positive and HPV-negative HNC cell lines were screened for cell viability upon treatment with SAHA, gefitinib and the combination of the two. Epithelial/mesenchymal marker expression, as well as activation of signalling pathway, were assessed upon SAHA treatment. ΔNp63α silencing with shRNA lentiviral particles was used to determine its role in cell proliferation, migration and TGFβ pathway activation.
resultsWe found that both SAHA and gefitinib have antitumour activity in both HPV-positive and HPV-negative HNC cell lines and that their combination has a synergistic effect in inhibiting cell growth. SAHA treatment reverts EMT and inhibits the expression of the transcription factor ΔNp63α. Suppression of ΔNp63α reduces EGFR protein levels and decreases cell proliferation and TGFβ-dependent migration in both HPV-positive and HPV-negative HNC cell lines.
conclusionsOur results, by giving a clear molecular mechanism at the basis of the antitumour activity of SAHA in HNC cell lines, provide a rationale for the clinical evaluation of SAHA in combination with gefitinib in both HPV-positive and HPV-negative HNC patients. Further knowledge is key to devising additional lines of combinatorial treatment strategies for this disease.
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