Identification and Characterization of Oncogenic SOS1 Mutations in Lung Adenocarcinoma
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Abstract
Lung adenocarcinomas are characterized by mutations in the receptor tyrosine kinase (RTK)/Ras/Raf pathway, with up to 75% of cases containing mutations in known driver genes. However, the driver alterations in the remaining cases are yet to be determined. Recent exome sequencing analysis has identified SOS1, encoding a guanine nucleotide exchange factor, as significantly mutated in lung adenocarcinomas lacking canonical oncogenic RTK/Ras/Raf pathway mutations. Here, we demonstrate that ectopic expression of lung adenocarcinoma–derived mutants of SOS1 induces anchorage-independent cell growth in vitro and tumor formation in vivo. Biochemical experiments suggest that these mutations lead to overactivation of the Ras pathway, which can be suppressed by mutations that disrupt either the Ras-GEF or putative Rac-GEF activity of SOS1. Transcriptional profiling reveals that the expression of mutant SOS1 leads to the upregulation of MYC target genes and genes associated with Ras transformation. Furthermore, we demonstrate that an AML cancer cell line harboring a lung adenocarcinoma–associated mutant SOS1 is dependent on SOS1 for survival and is also sensitive to MEK inhibition. Our work provides experimental evidence for the role of SOS1 as an oncogene and suggests a possible therapeutic strategy to target SOS1-mutated cancers. Implications: This study demonstrates that SOS1 mutations found in lung adenocarcinoma are oncogenic and that MEK inhibition may be a therapeutic avenue for the treatment of SOS1-mutant cancers.
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SOS1 has been labeled as a potential oncogenic driver, with the capability of tumorigenesis in vivo and the ability to activate both the RAS protein through a RAS-GEF and Myc target genes, as well as increase phosphorylation of MEK.
“SOS1 has been labeled as a potential oncogenic driver, with the capability of tumorigenesis in vivo and the ability to activate both the RAS protein through a RAS-GEF (guanine nucleotide exchange factor) and Myc target genes, as well as increase phosphorylation of MEK22.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [22]
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- Authors
- Cai, D., Choi, P. S., Gelbard, M., & Meyerson, M.
- Affiliations
- Broad Institute (US)
- Corresponding author
- Meyerson, Matthew
- Venue
- Molecular Cancer Research
- Published
- 2019-04-01
- Volume
- 17
- Issue
- 4
- Pages
- 1002-1012
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- PMC
- PMC6445719
- OpenAlex
- W2910048802
- Cited by
- 41
- References
- 64
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 6 · 2021: 14 · 2020: 6 · 2019: 1
- FWCI
- 4.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (K99 CA208028)
- National Cancer Institute (1R35CA197568)
- 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 › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- SOS1, lung adenocarcinoma, oncogenic mutations, Ras signaling, guanine nucleotide exchange factor, MYC target genes, MEK inhibition, driver mutations, tumor formation, anchorage-independent growth
- MeSH terms
- Adenocarcinoma of Lung, Animals, Humans, Lung Neoplasms, Mutation, Transfection, Up-Regulation, Proto-Oncogene Proteins c-myc, ras Proteins, SOS1 Protein, Gene Expression Profiling, NIH 3T3 Cells, Mice
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