ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010
Amphiregulin promotes resistance to gefitinib in nonsmall cell lung cancer cells by regulating Ku70 acetylation.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- APOBEC3 Activity Promotes the Survival and Evolution of Drug-Tolerant Persister Cells during EGFR Inhibitor Resistance in Lung Cancer.Cancer research communications · 2025Article
- Amivantamab efficacy in wild-type EGFR NSCLC tumors correlates with levels of ligand expression.NPJ precision oncology · 2024Article
- Review
- Particulate matter facilitates amphiregulin-dependent lung cancer proliferation through glutamine metabolism.International journal of biological sciences · 2024Article
- Histone deacetylases modulate resistance to the therapy in lung cancer.Frontiers in genetics · 2022Review
- EEF1A2 interacts with HSP90AB1 to promote lung adenocarcinoma metastasis via enhancing TGF-β/SMAD signalling.British journal of cancer · 2021Article
- Apoptosis Induction byHistone Deacetylase Inhibitors in Cancer Cells: Role of Ku70.International journal of molecular sciences · 2019Review
- Role of epidermal growth factor receptor in lung cancer and targeted therapies.American journal of cancer research · 2017Review
- Membrane-Tethered Intracellular Domain of Amphiregulin Promotes Keratinocyte Proliferation.The Journal of investigative dermatology · 2016Article
- Synergistic activity of vorinostat combined with gefitinib but not with sorafenib in mutant KRAS human non-small cell lung cancers and hepatocarcinoma.OncoTargets and therapy · 2016Article
- Article
- Is there a role for epidermal growth factor receptor tyrosine kinase inhibitors in epidermal growth factor receptor wild-type non-small cell lung cancer?World journal of clinical oncology · 2015Review
- Biomarkers of erlotinib response in non-small cell lung cancer tumors that do not harbor the more common epidermal growth factor receptor mutations.International journal of clinical and experimental pathology · 2015Article
- Effect of piperlongumine on drug resistance reversal in human retinoblastoma HXO-RB44/VCR and SO-Rb50/CBP cell lines.International journal of clinical and experimental pathology · 2015Article
- Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.American journal of cancer research · 2014Review
- The HDAC inhibitor, MPT0E028, enhances erlotinib-induced cell death in EGFR-TKI-resistant NSCLC cells.Cell death & disease · 2013Article
- Role of Ku70 and Bax in epigallocatechin-3-gallate-induced apoptosis of A549 cells in vivo.Oncology letters · 2013Article
- Amphiregulin promotes BAX inhibition and resistance to gefitinib in non-small-cell lung cancers.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple molecular resistance mechanisms reduce the efficiency of receptor tyrosine kinase inhibitors such as gefitinib in non-small cell lung cancer (NSCLC). We previously demonstrated that amphiregulin (Areg) inhibits gefitinib-induced apoptosis in NSCLC cells by inactivating the proapoptotic protein BAX. In this part of the investigation, we studied the molecular mechanisms leading to BAX inactivation. We show that Areg prevents gefitinib-mediated acetylation of Ku70. This augments the BAX-Ku70 interaction and therefore prevents BAX-mediated apoptosis. Accordingly, Areg or Ku70 knock down restore BAX activation and apoptosis in gefitinib-treated H358 cells in vitro. In addition, overexpression of the histone acetyltransferase (HAT) CREB-binding protein (CBP) or treatments with histone deacetylase (HDAC) inhibitors sensitize H358 cells to gefitinib. Moreover, a treatment with vorinostat, a HDAC inhibitor strongly sensitized tumors to gefitinib in vivo. These findings suggest new prospects in combining both HDAC and epidermal growth factor receptor inhibitors for the treatment of NSCLC.
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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.