ArticleOncotarget2017
IGF1R depletion facilitates MET-amplification as mechanism of acquired resistance to erlotinib in HCC827 NSCLC cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Drug Resistance in Late-Stage Epidermal Growth Factor Receptor (EGFR)-Mutant Non-Small Cell Lung Cancer Patients After First-Line Treatment with Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2025Review
- CRISPR/Cas9 gene editing: a novel strategy for fighting drug resistance in respiratory disorders.Cell communication and signaling : CCS · 2024Review
- CRISPR/Cas9-mediated silencing of CD44: unveiling the role of hyaluronic acid-mediated interactions in cancer drug resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Role of Insulin-like Growth Factor-1 Receptor in Tobacco Smoking-Associated Lung Cancer Development.Biomedicines · 2024Review
- Modern therapies of nonsmall cell lung cancer.Journal of applied genetics · 2023Review
- Genome-wide epigenetic and mRNA-expression profiling followed by CRISPR/Cas9-mediated gene-disruptions corroborate theTranslational lung cancer research · 2023Article
- Applications and advancements of CRISPR-Cas in the treatment of lung cancer.Frontiers in cell and developmental biology · 2023Review
- Applications of CRISPR-Cas9 for advancing precision medicine in oncology: from target discovery to disease modeling.Frontiers in genetics · 2023Review
- Applications of CRISPR/Cas technology against drug-resistant lung cancers: an update.Molecular biology reports · 2022Review
- Gene Expression Profiling as a Potential Tool for Precision Oncology in Non-Small Cell Lung Cancer.Cancers · 2021Review
- CRISPR-Cas deployment in non-small cell lung cancer for target screening, validations, and discoveries.Cancer gene therapy · 2021Review
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- CRISPR/Cas9 for overcoming drug resistance in solid tumors.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Review
- Frontiers of ctDNA, targeted therapies, and immunotherapy in non-small-cell lung cancer.Translational lung cancer research · 2020Review
- Understanding Lineage Plasticity as a Path to Targeted Therapy Failure inFrontiers in genetics · 2020Review
- EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies.Frontiers in oncology · 2019Review
- Acquisition of EGFR TKI resistance and EMT phenotype is linked with activation of IGF1R/NF-κB pathway in EGFR-mutant NSCLC.Oncotarget · 2017Article
- CRISPR/Cas9: A revolutionary genome editing tool for human cancers treatment.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EGFR-mutated non-small cell lung cancer patients experience relapse within 1-2 years of treatment with EGFR-inhibitors, such as erlotinib. Multiple resistance mechanisms have been identified including secondary EGFR-mutations, MET-amplification, and epithelial-mesenchymal transition (EMT). Previous studies have indicated a role of Insulin-like growth factor 1 receptor (IGF1R) in acquired resistance to EGFR-directed drugs as well as in EMT. In the present study, we have investigated the involvement of IGF1R in acquired high-dose erlotinib resistance in the EGFR-mutated lung adenocarcinoma cell line HCC827. We observed that IGF1R was upregulated in the immediate response to erlotinib and hyperactivated in erlotinib resistant HCC827 cells. Resistant cells additionally acquired features of EMT, whereas MET-amplification and secondary EGFR-mutations were absent. Using CRISPR/Cas9, we generated a HCC827(IGFR1-/-) cell line and subsequently investigated resistance development in response to high-dose erlotinib. Interestingly, HCC827(IGFR1-/-) cells were now observed to specifically amplify the MET gene. Additionally, we observed a reduced level of mesenchymal markers in HCC827(IGFR1-/-) indicating an intrinsic enhanced epithelial signature compared to HCC827 cells. In conclusion, our data show that IGF1R have an important role in defining selected resistance mechanisms in response to high doses of erlotinib.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.