ArticleMolecular oncology2017
Belinostat exerts antitumor cytotoxicity through the ubiquitin-proteasome pathway in lung squamous cell carcinoma.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Post-translational protein lactylation modification in lung cancer: an emerging targeted therapeutic strategy.Frontiers in immunology · 2026Review
- The anticancer effect of the HDAC inhibitor belinostat is enhanced by inhibitors of Bcl-xMolecular oncology · 2025Article
- Comprehensive characterization of respiratory genes based on a computational framework in pan-cancer to develop stratified treatment strategies.PLoS computational biology · 2025Article
- Research progress and applications of epigenetic biomarkers in cancer.Frontiers in pharmacology · 2024Review
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- CXCL1 Clone Evolution Induced by the HDAC Inhibitor Belinostat Might Be a Favorable Prognostic Indicator in Triple-Negative Breast Cancer.BioMed research international · 2021Article
- Diverse Roles of F-BoxProtein3 in Regulation of Various Cellular Functions.Frontiers in cell and developmental biology · 2021Review
- Tambulin Targets Histone Deacetylase 1 Inhibiting Cell Growth and Inducing Apoptosis in Human Lung Squamous Cell Carcinoma.Frontiers in pharmacology · 2020Article
- From molecular promise to preclinical results: HDAC inhibitors in the race for healthy aging drugs.EMBO molecular medicine · 2019Review
- Post-Translational Modifications in NETosis and NETs-Mediated Diseases.Biomolecules · 2019Review
- Immunoepigenetics Combination Therapies: An Overview of the Role of HDACs in Cancer Immunotherapy.International journal of molecular sciences · 2019Review
- Drugs Targeting Epigenetic Modifications and Plausible Therapeutic Strategies Against Colorectal Cancer.Frontiers in pharmacology · 2019Review
- Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas.International journal of medical sciences · 2019Review
- Differential Role of the RasGEFs Sos1 and Sos2 in Mouse Skin Homeostasis and Carcinogenesis.Molecular and cellular biology · 2018Article
- Association of Smoking, Alcohol Use, and Betel Quid Chewing with Epigenetic Aberrations in Cancers.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There have been advances in personalized therapy directed by molecular profiles in lung adenocarcinoma, but not in lung squamous cell carcinoma (SCC). The lack of actionable driver oncogenes in SCC has restricted the use of small-molecule inhibitors. Here, we show that SCC cell lines displayed differential sensitivities to belinostat, a pan-histone deacetylase inhibitor. Phosphoproteomic analysis of belinostat-treated SCC cells revealed significant downregulation of the MAPK pathway, along with the induction of apoptosis. In cisplatin-resistant cells that demonstrated aberrant MAPK activation, combined treatment with belinostat significantly inhibited cisplatin-induced ERK phosphorylation and exhibited strong synergistic cytotoxicity. Furthermore, belinostat transcriptionally upregulated the F-box proteins FBXO3 and FBXW10, which directly targeted son of sevenless (SOS), an upstream regulator of the MAPK pathway, for proteasome-mediated degradation. Supporting this, suppression of SOS/ERK pathway by belinostat could be abrogated by inhibiting proteasomal activity either with bortezomib or with siRNA knockdown of FBXO3/FBXW10. Taken together, these preclinical data offer a novel understanding of the epigenetic mechanism by which belinostat exerts its cytotoxicity and supports the combination with cisplatin in clinical settings for chemorefractory SCC tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.