Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers
Open accessAbstract
Mutant KRAS and c-MYC are oncogenic drivers and rational therapeutic targets for the treatment of pancreatic cancer. Although tumor growth and homeostasis are largely dependent on these oncogenes, a few residual cancer cells are able to survive the ablation of mutant KRAS and c-MYC. By performing a genome-wide gene expression analysis of in vivo-derived bulk tumor cells and residual cancer cells lacking the expression of mutant KRAS or c-MYC, we have identified an increase in autocrine IGF1/AKT signaling as a common survival mechanism in dormant cancer cells. The pharmacological inhibition of IGF-1R reduces residual disease burden and cancer recurrence, suggesting that this molecular pathway is crucial for the survival of cancer cells in the absence of the primary oncogenic drivers.
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In KRAS-mutated pancreatic ductal cancer cells, KRAS inhibition decreased c-Myc expression, upregulated the expression of a gene set associated with the IGF-1 pathway, and increased IGF-1R phosphorylation.
“In KRAS-mutated pancreatic ductal cancer cells, KRAS inhibition decreased c-Myc expression, upregulated the expression of a gene set associated with the IGF-1 pathway in gene array-based transcriptome analysis, and increased IGF-1R phosphorylation [41].”
From Epithelial-mesenchymal transition status is a remarkable biomarker for the combination treatment with avutometinib and defactinib in KRAS-mutated non-small cell lung cancer (2024) · cites this paper as [41]
The Results section on oncogenic KRAS ablation reports IGF1-pathway gene-set changes and increased IGF-1R phosphorylation in residual mouse tumor cells; a separate Results section reports increased receptor activation after KRAS knockdown in human pancreatic cancer cells. The gene-set analysis was RNA-Seq in the mouse model, not a gene-array analysis in the human cells. The paper describes a change in c-MYC expression after KRAS ablation but does not explicitly state its direction in the available passage. (LLM, conf=0.88)
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The underexplored complexity of pancreatic cancer: Early dissemination and quiescence
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Cancer Cells in Sleep Mode: Wake Them to Eliminate or Keep Them Asleep Forever?
Liu, W., Kovacs, A. H., & Hou, J. (2024) · Cells · doi:10.3390/cells13232022 · Cited by 2 · see citing works
From Worms to Tumors: Conserved Strategies of Cellular Arrest and Survival Governing Dormancy
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EHD4 and ASAP2 are critical negative regulators of the claudin‐5‐based endothelial barrier
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KRAS mutated lung adenocarcinoma responds to pan-ERBB and Aurora kinase inhibitors
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- Authors
- Rajbhandari, N., Lin, W.-C., Wehde, B. L., Triplett, A. A., & Wagner, K.-U.
- Affiliations
- Nebraska Medical Center (US)
- University of Nebraska Medical Center (US)
- Corresponding author
- Wagner, Kay-Uwe
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-02
- Volume
- 18
- Issue
- 9
- Pages
- 2243-2255
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5369772
- OpenAlex
- W2592443973
- Cited by
- 68
- References
- 30
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 6 · 2023: 6 · 2022: 7 · 2021: 15 · 2020: 4 · 2019: 9 · 2018: 7 · 2017: 1 · 2012: 1
- FWCI
- 2.53
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Nebraska Cancer and Smoking Disease Research Program (NE DHHS LB506 2011-36, LB506 2016-54)
- Public Health Service (CA202917, R21 CA155175)
- UNMC Graduate Studies Office
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- pancreatic cancer, tumor dormancy, IGF-1 receptor, Akt signaling, mutant KRAS, c-Myc, residual tumor cells, tumor recurrence, oncogenic drivers, gene expression profiling
- MeSH terms
- Animals, Humans, Insulin-Like Growth Factor I, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Neoplasm Recurrence, Local, Oncogenes, Pancreas, Pancreatic Neoplasms, Signal Transduction, Gene Expression, Genes, myc, Proto-Oncogene Proteins p21(ras), Receptor, IGF Type 1, Mice, Knockout, Autocrine Communication, Cell Line, Tumor, Cell Proliferation, Proto-Oncogene Proteins c-akt, Mice, Carcinogenesis
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