ArticleJTO clinical and research reports2024
Phosphoproteomic Analysis Identified Mutual Phosphorylation of FAK and Src as a Mechanism of Osimertinib Resistance in
Article in JTO clinical and research reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Recent advances in Pyrazolo[3,4-d]pyrimidine-based dual inhibitors in the treatment of cancers.Molecular diversity · 2026Review
- Review
- ACTN4 Gene Amplification and Actinin-4 Protein Expression for Osimertinib Efficacy in EGFR-Mutant NSCLC.Cancer science · 2025Article
- Multi-omics approaches including single-cell analysis and machine learning were used to identify the roles of telomere-related genes in esophageal squamous cell carcinoma.Discover oncology · 2025Article
- Panduratin A fromInternational journal of molecular sciences · 2025Article
- Novel FAK inhibitors suppress tumor growth and reverse EGFR-TKI resistance in non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 7 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Osimertinib is a standard treatment for patients with Methods: We established two osimertinib-resistant cell lines from Results: Phosphoproteomic analysis revealed 80 phosphorylation sites that were mutually up-regulated in PC-9OR and HCC827OR cells. The Kinase Enrichment Analysis version 3 analysis identified focal adhesion kinase (FAK) and proto-oncogene tyrosine-protein kinase Src (Src) as upstream kinases of these up-regulated phosphoproteins. The small-interfering RNA-mediated knockdown of FAK reduced Src phosphorylation and that of Src reduced FAK phosphorylation in both cell lines. Furthermore, FAK- or Src-specific small-interfering RNA treatments restored EGFR phosphorylation in PC-9OR and HCC827OR cells. The combination of FAK and Src inhibitors inhibited PC-9OR and HCC827OR cell proliferation in vitro and suppressed tumor growth in a xenograft mouse model. Immunohistochemistry of tumors from patients with Conclusions: Phosphoproteomic analysis may help elucidate the mechanisms of resistance to molecular-targeted therapies in lung cancer. Mutual phosphorylation of FAK and Src is involved in osimertinib resistance. Thus, FAK and Src inhibition may be novel treatment strategies for osimertinib-resistant NSCLC.
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Registered trials
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