Cell Type–Specific Adaptive Signaling Responses to KRASG12C Inhibition
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Abstract
Purpose: Covalent inhibitors of KRASG12C specifically target tumors driven by this form of mutant KRAS, yet early studies show that bypass signaling drives adaptive resistance. Although several combination strategies have been shown to improve efficacy of KRASG12C inhibitors (KRASi), underlying mechanisms and predictive strategies for patient enrichment are less clear. Experimental Design: We performed mass spectrometry–based phosphoproteomics analysis in KRASG12C cell lines after short-term treatment with ARS-1620. To understand signaling diversity and cell type–specific markers, we compared proteome and phosphoproteomes of KRASG12C cells. Gene expression patterns of KRASG12C cell lines and lung tumor tissues were examined. Results: Our analysis suggests cell type–specific perturbation to ERBB2/3 signaling compensates for repressed ERK and AKT signaling following ARS-1620 treatment in epithelial cell type, and this subtype was also more responsive to coinhibition of SHP2 and SOS1. Conversely, both high basal and feedback activation of FGFR or AXL signaling were identified in mesenchymal cells. Inhibition of FGFR signaling suppressed feedback activation of ERK and mTOR, while AXL inhibition suppressed PI3K pathway. In both cell lines and human lung cancer tissues with KRASG12C, we observed high basal ERBB2/3 associated with epithelial gene signatures, while higher basal FGFR1 and AXL were observed in cells/tumors with mesenchymal gene signatures. Conclusions: Our phosphoproteomic study identified cell type–adaptive responses to KRASi. Markers and targets associated with ERBB2/3 signaling in epithelial subtype and with FGFR1/AXL signaling in mesenchymal subtype should be considered in patient enrichment schemes with KRASi.
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A mesenchymal-like differentiation state can act as a resistance mechanism to KRAS inhibitors.
“A mesenchymal-like differentiation state can act as a resistance mechanism to KRAS inhibitors [126,128,130].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [128]
Phosphoproteomic studies on NSCLC cells treated with KRAS inhibitors identified upregulation of ERBB2/3 and AXL.
“Finally, phosphoproteomic studies on NSCLC cells treated with KRAS inhibitors identified several additional activated pathways including the upregulation of ERBB2/3 and AXL [128].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [128]
Phospho-proteomics analysis revealed that ERBB2/3 signaling mediates an adaptive response to KRAS G12C inhibition in epithelial cells, while feedback activation of FGFR and AXL was found in mesenchymal cells.
“Phospho-proteomics analysis revealed that ERBB2/3 signaling mediates an adaptive response to KRAS G12C inhibition in epithelial cells, while feedback activation of FGFR and AXL was found in mesenchymal cells [78].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [78]
RTKs were implicated in resistance to KRAS G12C inhibition associated with epithelial-mesenchymal transition.
“RTKs were also implicated in resistance to KRAS G12C inhibition associated with epithelial-mesenchymal transition (EMT) [77, 78].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [78]
High basal ERBB2/3 associated with epithelial gene signatures was observed in KRAS (G12C) cell lines and human lung cancers.
“High basal ERBB2/3 associated with epithelial gene signatures was observed in KRAS (G12C) cell lines and human lung cancers.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [131]
This changed cell type is more sensitive to co-inhibition by SHP2 and SOS1.
“This changed cell type is more sensitive to co-inhibition by SHP2 and SOS1 [130–135].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [131]
The IGF1R/ERBB2/3 signaling pathway may respond to the suppressed ERK and AKT signaling after KRAS (G12C) inhibitor treatment and favor the change to epithelial cell types.
“The IGF1R/ERBB2/3 signaling pathway may respond to the suppressed ERK and AKT signaling after KRAS (G12C) inhibitor treatment and favor the change to epithelial cell types (Fig. 5).”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [131]
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- Authors
- Solanki, H. S., Welsh, E. A., Fang, B., Izumi, V., Darville, L., Stone, B., Franzese, R., Chavan, S., Kinose, F., Imbody, D., Koomen, J. M., Rix, U., & Haura, E. B.
- Affiliations
- Moffitt Cancer Center (US)
- University of South Florida (US)
- Corresponding author
- Haura, Eric B.
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2021-02-22
- Volume
- 27
- Issue
- 9
- Pages
- 2533-2548
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC9940280
- OpenAlex
- W3130115867
- Cited by
- 106
- References
- 50
- Citations by year
- 2026: 17 · 2025: 25 · 2024: 25 · 2023: 19 · 2022: 10 · 2021: 10
- FWCI
- 5.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- State of Florida Bankhead Coley (5BC07)
- H. Lee Moffitt Cancer Center and Research Institute (P30-CA076292)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- KRAS G12C, KRAS inhibitors, adaptive resistance, bypass signaling, phosphoproteomics, FGFR1, AXL, SHP2, SOS1, PI3K signaling, mTOR, lung cancer, patient enrichment, combination therapy
- MeSH terms
- Alleles, Chromatography, Liquid, Humans, Mutation, Phosphoproteins, Piperazines, Quinazolines, Biomarkers, Tumor, Signal Transduction, Proto-Oncogene Proteins p21(ras), Receptor, ErbB-2, Erb-b2 Receptor Tyrosine Kinases, Computational Biology, Amino Acid Substitution, Receptor, ErbB-3, Protein Interaction Mapping, Proteomics, Cell Line, Tumor, Receptor, Fibroblast Growth Factor, Type 1, Tandem Mass Spectrometry, Epithelial-Mesenchymal Transition, Protein Interaction Maps
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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