ArticleCancer chemotherapy and pharmacology2013
Inhibiting proliferation of gefitinib-resistant, non-small cell lung cancer.
Article in Cancer chemotherapy and pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- MiR-23c Regulates the Resistance to Gefitinib in EGFR Mutant Non-Small-Cell Lung Cancer Cells.Cells · 2026Article
- Osimertinib-resistant NSCLC cells activate ERBB2 and YAP/TAZ and are killed by neratinib.Biochemical pharmacology · 2021Article
- FGFC1 Selectively Inhibits Erlotinib-Resistant Non-Small Cell Lung CancerFrontiers in pharmacology · 2021Article
- RNF25 promotes gefitinib resistance in EGFR-mutant NSCLC cells by inducing NF-κB-mediated ERK reactivation.Cell death & disease · 2018Article
- In Vitro Drug Sensitivity Tests to Predict Molecular Target Drug Responses in Surgically Resected Lung Cancer.PloS one · 2016Article
- In Situ Characterizing Membrane Lipid Phenotype of Human Lung Cancer Cell Lines Using Mass Spectrometry Profiling.Journal of Cancer · 2016Article
- Short-hairpin RNA library: identification of therapeutic partners for gefitinib-resistant non-small cell lung cancer.Oncotarget · 2015Article
- Belinostat: first global approval.Drugs · 2014Article
- Epidermal growth factor receptor (EGFR) signaling regulates global metabolic pathways in EGFR-mutated lung adenocarcinoma.The Journal of biological chemistry · 2014Article
- Molecular pathways and therapeutic targets in lung cancer.Oncotarget · 2014Review
- Celastrol induces apoptosis in gefitinib-resistant non-small cell lung cancer cells via caspases-dependent pathways and Hsp90 client protein degradation.Molecules (Basel, Switzerland) · 2014Article
- Laminin-5γ-2 (LAMC2) is highly expressed in anaplastic thyroid carcinoma and is associated with tumor progression, migration, and invasion by modulating signaling of EGFR.The Journal of clinical endocrinology and metabolism · 2014Article
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
purposeSensitivity to a tyrosine kinase inhibitor (TKI) is correlated with the presence of somatic mutations that affect the kinase domain of epidermal growth factor receptor (EGFR). Development of resistance to TKI is a major therapeutic problem in non-small cell lung cancer (NSCLC). Aim of this study is to identify agents that can overcome TKI resistance in NSCLC.
methodsWe used a carefully selected panel of 12 NSCLC cell lines to address this clinical problem. Initially, the cell lines were treated with a variety of 10 compounds. Cellular proliferation was measured via MTT assay. We then focused on the gefitinib-resistant, EGFR mutant cell lines [H1650: exon 19 and PTEN mutations; and H1975: exons 20 (T790M) and 21 (L858R)] to identify agents that could overcome TKI resistance.
resultsBoth 17-DMAG (Hsp90 inhibitor) and belinostat (histone deacetylase inhibitor, HDACi) effectively decreased the growth of almost all NSCLC lines. Also, belinostat markedly decreased the expression of EGFR and phospho-Akt in the cells. Combination of 17-DMAG and belinostat synergistically inhibited in vitro proliferation of these cells. Furthermore, both agents and their combination almost completely prevented TKI-resistant tumor formation (EGFR T790M mutation) in a xenograft model.
conclusionThese results suggest that the combination of 17-DMAG and belinostat should be examined in a clinical trial for TKI-resistant NSCLC cell.
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