Cited by 111Lung Cancer Treatments and MutationsProtein Kinase Regulation and GTPase SignalingMelanoma and MAPK Pathways

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The ERBB network facilitates KRAS-driven lung tumorigenesis

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Kruspig, Björn, Monteverde, Tiziana, Neidler, Sarah, Hock, Andreas, Kerr, Emma, Nixon, Colin, Clark, William, Hedley, Ann, Laing, Sarah, Coffelt, Seth B., Le Quesne, John, Dick, Craig, Vousden, Karen H., Martins, Carla P., Murphy, Daniel J.·2018·Science Translational Medicine

DOI 10.1126/scitranslmed.aao2565PMC PMC6881183

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Abstract

Abstract KRAS is the most frequently mutated driver oncogene in human adenocarcinoma of the lung. There are presently no clinically proven strategies for treatment of KRAS-driven lung cancer. Activating mutations in KRAS are thought to confer independence from upstream signaling, however recent data suggest that this independence may not be absolute. Here we show that initiation and progression of KRAS-driven lung tumors requires input from ERBB family RTKs: Multiple ERBB RTKs are expressed and active from the earliest stages of KRAS driven lung tumor development, and treatment with a multi-ERBB inhibitor suppresses formation of KRas G12D -driven lung tumors. We present evidence that ERBB activity amplifies signaling through the core RAS pathway, supporting proliferation of KRAS mutant tumor cells in culture and progression to invasive disease in vivo . Importantly, brief pharmacological inhibition of the ERBB network significantly enhances the therapeutic benefit of MEK inhibition in an autochthonous tumor setting. Our data suggest that lung cancer patients with KRAS-driven disease may benefit from inclusion of multi-ERBB inhibitors in rationally designed treatment strategies. One Sentence Summary G12 Mutant KRAS requires tonic ERBB network activity for initiation and maintenance of lung cancer

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Authors: Kruspig, B., Monteverde, T., Neidler, S., Hock, A., Kerr, E., Nixon, C., Clark, W., Hedley, A., Laing, S., Coffelt, S. B., Le Quesne, J., Dick, C., Vousden, K. H., Martins, C. P., & Murphy, D. J.
Affiliations: University of Glasgow (GB)
Cancer Research UK Scotland Institute (GB)
MRC Cancer Unit (GB)
MRC Toxicology Unit, Leicester LE1 7HB, UK.
National Health Service (GB)
Corresponding author: Kruspig, Björn
Monteverde, Tiziana
Murphy, Daniel J.
ORCID: Kruspig, Björn
Monteverde, Tiziana
Neidler, Sarah
Kerr, Emma
Nixon, Colin
Clark, William
Hedley, Ann
Laing, Sarah
Coffelt, Seth B.
Le Quesne, John
Vousden, Karen H.
Martins, Carla P.
Murphy, Daniel J.
Venue: Science Translational Medicine
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2018-06-20
Volume: 10
Issue: 446
ISSN: 1946-6234 (ISSN-L)
1946-6242
DOI: 10.1126/scitranslmed.aao2565
PMC: PMC6881183
OpenAlex: W2809593667
Cited by: 111
References: 47
Citations by year: 2026: 7 · 2025: 14 · 2024: 8 · 2023: 12 · 2022: 14 · 2021: 19 · 2020: 16 · 2019: 15 · 2018: 6
FWCI: 10.54
Type: journal article
Language: en
Open access: green
doi.org
Locations: Science Translational Medicine (publishedVersion)
bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion, cc-by-sa)
Funders: Medical Research Council (5TS30)
British Lung Foundation (APHD13-5, CSOBLF RG16-2)
European Commission (CIG 618448, 705190 “NuSiCC”)
Deutsche Krebshilfe (109220)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Keywords: KRAS mutation, lung cancer, lung carcinogenesis, Ras signaling, MEK inhibition, combination therapy, tumor progression, cell proliferation
MeSH terms: Adenocarcinoma of Lung, Animals, Humans, Lung Neoplasms, Mutation, Phosphorylation, Signal Transduction, Gene Expression Regulation, Neoplastic, Survival Analysis, Proto-Oncogene Proteins p21(ras), Apoptosis, Disease Progression, Mitogen-Activated Protein Kinase Kinases, Cell Line, Tumor, Extracellular Signal-Regulated MAP Kinases, Cell Proliferation, Mice, Gene Regulatory Networks, Carcinogenesis, ErbB Receptors

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The ERBB network facilitates KRAS-driven lung tumorigenesis

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