ArticleCell death & disease2022
EGFL7 drives the evolution of resistance to EGFR inhibitors in lung cancer by activating NOTCH signaling.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- EGFL7 Inhibits the Immune Response in Metastatic Castration-Resistant Prostate Cancer by Deactivating Endothelial Intercellular Adhesion Molecule-1.The world journal of men's health · 2026Article
- Multi-omics analysis reveals RBPJ-mediated regulation of EGF/ACTN2/MYPN/COL21A1 in fibroblast during oviduct functional remodeling of duck.Poultry science · 2026Article
- Article
- Comprehensive analysis of Mendelian randomization and scRNA-seq identify key prognostic genes and relevant functional roles in colorectal cancer.Scientific reports · 2025Article
- Identification of key regulators in pancreatic ductal adenocarcinoma using network theoretical approach.PloS one · 2025Article
- The strategies to cure cancer patients by eradicating cancer stem-like cells.Molecular cancer · 2023Review
- Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
- Nano-Enabled Strategies for the Treatment of Lung Cancer: Potential Bottlenecks and Future Perspectives.Biomedicines · 2023Review
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence supports evolutionary trait of drug resistance. Like resilience in other systems, most tumor cells experience drug-tolerant state before full resistance acquired. However, the underlying mechanism is still poorly understood. Here, we identify that EGF like domain multiple 7 (EGFL7) is a responsive gene to epidermal growth factor receptor (EGFR) kinase inhibition during a period when tumors are decimated. Moreover, our data reveal that the adaptive increase of EGFL7 during this process is controlled by the depression of nonsense-mediated mRNA decay (NMD) pathway. Upregulation of EGFL7 activates NOTCH signaling in lung cancer cells, which slows down the decrease of c-Myc caused by EGFR inhibition, thereby helping the survival of cancer cells. Our data, taken together, demonstrate that EGFL7 is a driver gene for resistance to EGFR kinase inhibition, and suggest that targeting EGFL7/NOTCH signaling may improve the clinical benefits of EGFR inhibitors in patients with EGFR mutant tumors.
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