ArticleiScience2024
AXL and SHC1 confer crizotinib resistance in patient-derived xenograft model of ALK-driven lung cancer.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Supercharged ferritin nanocages enable universal cytosolic protein delivery.Nature communications · 2026Article
- [Role of Receptor Tyrosine Kinase AXL in Cancer Targeted Therapy Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Article
- Glucocorticoid inhibits lung cancer cells proliferation and migration by suppressing smad2/3 activation.Scientific reports · 2025Article
- Prognostic implication of endoplasmic reticulum stress-related gene signature in lung adenocarcinoma and its effect on tumor immunity.Translational cancer research · 2025Article
- Construction and validation of an EGFR-related risk signature identifiedTranslational cancer research · 2025Article
- Identification and verification of immune and oxidative stress-related diagnostic indicators for malignant lung nodules through WGCNA and machine learning.Scientific reports · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Anaplastic lymphoma kinase (ALK) inhibitor crizotinib has dramatic effect in non-small cell lung cancer patients with ALK rearrangement. However, most patients eventually develop resistance. To discover therapeutic targets to overcome crizotinib resistance (CR), we generated patient-derived xenograft CR mice and subjected them to phosphorylation profiling, together with CR mice treated with ASP3026 or alectinib. We identified 100 proteins with different phosphorylation status in CR mice. Among them, AXL phosphorylation was increased in CR mice, which could not be reversed by ASP3026 or alectinib. Importantly, the combined treatment of crizotinib and AXL inhibitor in CR mice significantly inhibited tumor growth, compared to crizotinib alone. We also found that SHC1 phosphorylation was increased in CR mice and SHC1 knockdown sensitized ALK-driven cells to crizotinib. Our study provides a new view of signaling pathways leading to CR, suggesting AXL and SHC1 as potential targets for combination therapy to overcome CR.
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