ArticleCell death & disease2019
Targeting HDAC/OAZ1 axis with a novel inhibitor effectively reverses cisplatin resistance in non-small cell lung cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Review
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- DNA Damage Repair in Glioblastoma: A Novel Approach to Combat Drug Resistance.Cell proliferation · 2025Article
- 3D genome organization shapes DNA damage susceptibility to platinum-based drugs.Nucleic acids research · 2025Article
- Histone Deacetylase Inhibitors Promote the Anticancer Activity of Cisplatin: Mechanisms and Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Biological Significance and Therapeutic Promise of Programmed Ribosomal Frameshifting.International journal of molecular sciences · 2025Review
- A short overview of dual targeting HDAC inhibitors.Future medicinal chemistry · 2025Article
- Trichostatin A Promotes Cytotoxicity of Cisplatin, as Evidenced by Enhanced Apoptosis/Cell Death Markers.Molecules (Basel, Switzerland) · 2024Article
- Deep Learning Techniques to Characterize theBiomedicines · 2024Article
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Gain-of-function mutations in the catalytic domain ofScience advances · 2023Article
- HDAC-an important target for improving tumor radiotherapy resistance.Frontiers in oncology · 2023Review
- Differentiation-related genes in tumor-associated macrophages as potential prognostic biomarkers in non-small cell lung cancer.Frontiers in immunology · 2023Article
- Development of a polyamine gene expression score for predicting prognosis and treatment response in clear cell renal cell carcinoma.Frontiers in immunology · 2022Article
- Identifying enhancer-driven subtype-specific prognostic markers in breast cancer based on multi-omics data.Frontiers in immunology · 2022Article
- Histone deacetylases modulate resistance to the therapy in lung cancer.Frontiers in genetics · 2022Review
- PaDef (Frontiers in molecular biosciences · 2022Article
- In silico model for miRNA-mediated regulatory network in cancer.Briefings in bioinformatics · 2021Article
- Role of Antizyme Inhibitor Proteins in Cancers and Beyond.OncoTargets and therapy · 2021Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin yields significant efficacy and is generally used as a frontline therapy for non-small cell lung cancer (NSCLC). However, acquired resistance strongly limits its application. Here, we identified that a novel histone deacetylase (HDAC) inhibitor S11, with P-glycoprotein inhibitory activity, could obviously suppress cell growth in cisplatin-resistant NSCLC cell lines. In addition, S11 could increase the expression of Ac-H4 and p21, which confirmed its HDAC inhibitory action, suppress colony formation, and block cell migration of cisplatin-resistant NSCLC cells. Notably, co-treatment with S11 and cisplatin exhibited synergistically inhibitory efficacy in cisplatin-resistant NSCLC cells. Gene microarray data showed that OAZ1 was downregulated in resistant cells but upregulated after S11 treatment. Further study indicated that knockdown of OAZ1 by siRNA resulted in the decrease of sensitivity of resistant cells to cisplatin treatment and contributed to the increase of resistant cell migration. Additionally, ChIP assay data demonstrated that HDAC inhibitor S11 could increase the accumulation of Ac-H4 in OAZ1 promoter region, suggesting the direct regulation of OAZ1 by HDAC. Importantly, the combination of S11 and cisplatin overcome resistance through inhibiting HDAC activity and subsequently increasing the OAZ1 expression in preclinical model. Moreover, we observed that positive expression of HDAC1 was associated with the downregulation of OAZ1 in NSCLC patients with platinum-based treatment, and predicted drug resistance and poor prognosis. In summary, we demonstrated a role of HDAC/OAZ1 axis in cisplatin-resistant NSCLC and identified a promising compound to overcome cisplatin resistance.
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