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FAS and NF-κB signalling modulate dependence of lung cancers on mutant EGFR
Open accessAbstract
Human lung adenocarcinomas with activating mutations in EGFR (epidermal growth factor receptor) often respond to treatment with EGFR tyrosine kinase inhibitors (TKIs), but the magnitude of tumour regression is variable and transient. This heterogeneity in treatment response could result from genetic modifiers that regulate the degree to which tumour cells are dependent on mutant EGFR. Through a pooled RNA interference screen, we show that knockdown of FAS and several components of the NF-κB pathway specifically enhanced cell death induced by the EGFR TKI erlotinib in EGFR-mutant lung cancer cells. Activation of NF-κB through overexpression of c-FLIP or IKK (also known as CFLAR and IKBKB, respectively), or silencing of IκB (also known as NFKBIA), rescued EGFR-mutant lung cancer cells from EGFR TKI treatment. Genetic or pharmacologic inhibition of NF-κB enhanced erlotinib-induced apoptosis in erlotinib-sensitive and erlotinib-resistant EGFR-mutant lung cancer models. Increased expression of the NF-κB inhibitor IκB predicted for improved response and survival in EGFR-mutant lung cancer patients treated with EGFR TKI. These data identify NF-κB as a potential companion drug target, together with EGFR, in EGFR-mutant lung cancers and provide insight into the mechanisms by which tumour cells escape from oncogene dependence.
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“In erlotinib-sensitive and erlotinib-resistant EGFR-mutant lung cancer models, genetic or pharmacologic inhibition of NF-κB increased erlotinib-induced apoptosis [114].”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [114]
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Self-citation
Metadata
- Authors
- Bivona, T. G., Hieronymus, H., Parker, J., Chang, K., Taron, M., Rosell, R., Moonsamy, P., Dahlman, K., Miller, V. A., Costa, C., Hannon, G., & Sawyers, C. L.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cold Spring Harbor Laboratory (US)
- Institut Català d'Oncologia (ES)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Sawyers, Charles L.
- ORCID
- Venue
- Nature
- Published
- 2011-03
- Volume
- 471
- Issue
- 7339
- Pages
- 523-526
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3541675
- OpenAlex
- W2087955215
- Cited by
- 396
- References
- 24
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 8 · 2023: 14 · 2022: 20 · 2021: 19 · 2020: 17 · 2019: 33 · 2018: 46 · 2017: 38 · 2016: 25 · 2015: 27 · 2014: 37 · 2013: 37 · 2012: 39
- FWCI
- 37.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Memorial Sloan-Kettering Cancer Center
- National Cancer Institute (P01CA013106)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- NF-κB signaling, erlotinib, EGFR tyrosine kinase inhibitors, drug resistance, IκB, c-FLIP, IκB kinase, RNAi screen, lung adenocarcinoma, apoptosis, combination therapy, treatment response biomarkers, non-smoker lung cancer
- MeSH terms
- Erlotinib Hydrochloride, Dose-Response Relationship, Drug, Humans, Lung Neoplasms, Models, Biological, Mutation, Quinazolines, Signal Transduction, Down-Regulation, NF-kappa B, Genes, erbB-1, Drug Resistance, Neoplasm, fas Receptor, I-kappa B Proteins, RNA Interference, Cell Line, Tumor, Mutant Proteins, ErbB Receptors
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