ArticleScientific reports2021
Contribution of p53 in sensitivity to EGFR tyrosine kinase inhibitors in non-small cell lung cancer.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
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- Silencing of NUP62 overcomes osimertinib resistance via ubiquitination of survivin in non-small cell lung cancer cells.British journal of cancer · 2026Article
- Early-Phase Activation of Epithelial-Mesenchymal Transition in Lung Cancer Cells Treated with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Article
- Association of TP53 gain-of-function mutations with early osimertinib resistance in epidermal growth factor receptor-mutant lung adenocarcinoma.ESMO open · 2026Article
- Prime Editing, CRISPR-Cas9, and NanoCas Genome Editing for Cancer Treatment.Molecular biotechnology · 2026Review
- Lung-molGPA may stratify the prognostic impact of TP53 co-mutation in EGFR-mutant lung adenocarcinoma with brain metastases: a multi-center retrospective analysis.Therapeutic advances in medical oncology · 2026Article
- Current and Emerging Therapies for Targeting the ERK1/2 & PI3K Pathways in Cancer.International journal of molecular sciences · 2025Review
- Cholesterol Regulates Airway Epithelial Cell Differentiation by Inhibiting p53 Nuclear Translocation.International journal of molecular sciences · 2025Article
- Optimizing Osimertinib for NSCLC: Targeting Resistance and Exploring Combination Therapeutics.Cancers · 2025Review
- Silibinin-Loaded Amphiphilic PLGA-Poloxamer Nanoparticles: Physicochemical Characterization, Release Kinetics, and Bioactivity Evaluation in Lung Cancer Cells.Materials (Basel, Switzerland) · 2024Article
- CRISPR-mediated ablation of TP53 and EGFR mutations enhances gefitinib sensitivity and anti-tumor efficacy in lung cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Two-polarized roles of transcription factor FOSB in lung cancer progression and prognosis: dependent on p53 status.Journal of experimental & clinical cancer research : CR · 2024Article
- p53 activation enhances the sensitivity of non-small cell lung cancer to the combination of SH003 and docetaxel by inhibiting de novo pyrimidine synthesis.Cancer cell international · 2024Article
- Comprehensive review of CRISPR-based gene editing: mechanisms, challenges, and applications in cancer therapy.Molecular cancer · 2024Review
- ITGB1 and DDR activation as novel mediators in acquired resistance to osimertinib and MEK inhibitors in EGFR-mutant NSCLC.Scientific reports · 2024Article
- Activity of afatinib in patients with NSCLC harboring novel uncommonFrontiers in oncology · 2024Article
- Epidermal growth factor receptor-mutated lung carcinomas with insufficient response to epidermal growth factor receptor inhibitors.Future oncology (London, England) · 2024Review
- Role and therapeutic targeting of glutamine metabolism in non‑small cell lung cancer (Review).Oncology letters · 2023Review
- Tp53 haploinsufficiency is involved in hotspot mutations and cytoskeletal remodeling in gefitinib-induced drug-resistant EGFRCell death discovery · 2023Article
- Long-lasting benefit on multimodal treatment combining osimertinib and stereotaxic radiotherapy for metastatic non-small cell lung cancer with the EGFR exon 20 insertion 773-774 HVdelinsLM: a case report.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The emergence of resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) with activating EGFR mutations is a major hindrance to treatment. We investigated the effects of p53 in primary sensitivity and acquired resistance to EGFR-TKIs in NSCLC cells. Changes in sensitivity to EGFR-TKIs were determined using p53 overexpression or knockdown in cells with activating EGFR mutations. We investigated EMT-related molecules, morphologic changes, and AXL induction to elucidate mechanisms of acquired resistance to EGFR-TKIs according to p53 status. Changes in p53 status affected primary sensitivity as well as acquired resistance to EGFR-TKIs according to cell type. Firstly, p53 silencing did not affect primary and acquired resistance to EGFR-TKIs in PC-9 cells, but it led to primary resistance to EGFR-TKIs through AXL induction in HCC827 cells. Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells. Furthermore, two cell lines (H1975 and H1975/p53
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