NF-κB-Activating Complex Engaged in Response to EGFR Oncogene Inhibition Drives Tumor Cell Survival and Residual Disease in Lung Cancer

Blakely, Collin M.; Pazarentzos, Evangelos; Olivas, Victor; Asthana, Saurabh; Yan, Jenny Jiacheng; Tan, Irena; Hrustanovic, Gorjan; Chan, Elton; Lin, Luping; Neel, Dana S.; Newton, William; Bobb, Kathryn L.; Fouts, Timothy R.; Meshulam, Jeffrey; Gubens, Matthew A.; Jablons, David M.; Johnson, Jeffrey R.; Bandyopadhyay, Sourav; Krogan, Nevan J.; Bivona, Trever G.

doi:10.1016/j.celrep.2015.03.012

Cited by 204Lung Cancer Treatments and MutationsNF-κB Signaling PathwaysHER2/EGFR in Cancer Research

NF-κB-Activating Complex Engaged in Response to EGFR Oncogene Inhibition Drives Tumor Cell Survival and Residual Disease in Lung Cancer

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Blakely, Collin M., Pazarentzos, Evangelos, Olivas, Victor, Asthana, Saurabh, Yan, Jenny Jiacheng, Tan, Irena, Hrustanovic, Gorjan, Chan, Elton +12 more·2015·Cell Reports

DOI 10.1016/j.celrep.2015.03.012PMC PMC4394036

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Abstract

Although oncogene-targeted therapy often elicits profound initial tumor responses in patients, responses are generally incomplete because some tumor cells survive initial therapy as residual disease that enables eventual acquired resistance. The mechanisms underlying tumor cell adaptation and survival during initial therapy are incompletely understood. Here, through the study of EGFR mutant lung adenocarcinoma, we show that NF-κB signaling is rapidly engaged upon initial EGFR inhibitor treatment to promote tumor cell survival and residual disease. EGFR oncogene inhibition induced an EGFR-TRAF2-RIP1-IKK complex that stimulated an NF-κB-mediated transcriptional survival program. The direct NF-κB inhibitor PBS-1086 suppressed this adaptive survival program and increased the magnitude and duration of initial EGFR inhibitor response in multiple NSCLC models, including a patient-derived xenograft. These findings unveil NF-κB activation as a critical adaptive survival mechanism engaged by EGFR oncogene inhibition and provide rationale for EGFR and NF-κB co-inhibition to eliminate residual disease and enhance patient responses.

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NF-κB signaling is rapidly engaged upon initial EGFR inhibitor treatment leading to activation of an NF-κB-mediated transcriptional survival program.
“In a follow-up study, they showed that NF-κB signaling is rapidly engaged upon initial EGFR inhibitor treatment leading to activation of an NF-κB-mediated transcriptional survival program [90].”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [90]

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Authors: Blakely, C. M., Pazarentzos, E., Olivas, V., Asthana, S., Yan, J. J., Tan, I., Hrustanovic, G., Chan, E., Lin, L., Neel, D. S., Newton, W., Bobb, K. L., Fouts, T. R., Meshulam, J., Gubens, M. A., Jablons, D. M., Johnson, J. R., Bandyopadhyay, S., Krogan, N. J., & Bivona, T. G.
Affiliations: University of California, San Francisco (US)
Gladstone Institutes (US)
Corresponding author: Bivona, Trever G.
ORCID: Blakely, Collin M.
Pazarentzos, Evangelos
Yan, Jenny Jiacheng
Tan, Irena
Lin, Luping
Neel, Dana S.
Fouts, Timothy R.
Gubens, Matthew A.
Johnson, Jeffrey R.
Bandyopadhyay, Sourav
Krogan, Nevan J.
Bivona, Trever G.
Venue: Cell Reports
Publisher: Elsevier BV
Published: 2015-04
Volume: 11
Issue: 1
Pages: 98-110
ISSN: 2211-1247 (ISSN-L)
DOI: 10.1016/j.celrep.2015.03.012
PMC: PMC4394036
OpenAlex: W2044246917
Cited by: 204
References: 57
Citations by year: 2026: 15 · 2025: 13 · 2024: 19 · 2023: 17 · 2022: 17 · 2021: 21 · 2020: 19 · 2019: 19 · 2018: 21 · 2017: 20 · 2016: 15 · 2015: 7
FWCI: 16.61
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Cell Reports (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Howard Hughes Medical Institute
Sidney Kimmel Foundation for Cancer Research
Bonnie J. Addario Lung Cancer Foundation
California Institute for Quantitative Biosciences
Searle Scholars Program
Servier
National Institutes of Health
National Heart, Lung, and Blood Institute (T32HL007185)
National Cancer Institute (CA174497, R01CA169338, DP2CA174497, K08CA154787)
National Institute of General Medical Sciences (P50GM082250, P50GM081879, R01GM107671)
National Institute of Allergy and Infectious Diseases (P01AI090935, P30AI027763)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
Keywords: NF-κB signaling, EGFR inhibition, EGFR-mutant lung adenocarcinoma, non-small cell lung cancer, TRAF2, RIPK1, IKK complex, tumor cell survival, residual disease, acquired drug resistance, CO inhibition, patient-derived xenografts
MeSH terms: Adenocarcinoma of Lung, Adenocarcinoma, Antineoplastic Agents, Cell Survival, Cyclohexanones, Epoxy Compounds, Humans, Lung Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, RNA-Binding Proteins, Apoptosis, Drug Resistance, Neoplasm, Nuclear Pore Complex Proteins, Cell Line, Tumor, TNF Receptor-Associated Factor 2, Proto-Oncogene Proteins c-akt, I-kappa B Kinase, Molecular Targeted Therapy, ErbB Receptors

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NF-κB-Activating Complex Engaged in Response to EGFR Oncogene Inhibition Drives Tumor Cell Survival and Residual Disease in Lung Cancer

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