ArticleActa pharmacologica Sinica2021
TGFβ2-mediated epithelial-mesenchymal transition and NF-κB pathway activation contribute to osimertinib resistance.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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52 citing papers in PubMed, 59 citations in OpenAlex.
- Baicalin-Chlorogenic Acid Self-Assembled Nanoparticles: A Carrier-Free Nano-Formulation for the Treatment of Acute Pharyngitis.Biomedicines · 2026Article
- Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.MedComm · 2026Review
- Reciprocal signaling-metabolic crosstalk between fibroblasts and tumor cells drives cetuximab tolerance in head and neck cancers.Journal of experimental & clinical cancer research : CR · 2026Article
- Precision Medicine in Treating Lung Cancer: A Narrative Review on Treatments Targeting Oncogenic Genetic Mutations.Cureus · 2026Review
- LINC00886 inhibits the proliferation, migration, and invasion of NSCLC cells by sponging miR-141-5p.Discover oncology · 2026Article
- Targeting dormant cancer cells: ferroptosis as a precision therapeutic strategy.Cellular & molecular biology letters · 2026Review
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Traditional Chinese medicine reprograms the tumor microenvironment to overcome EGFR-TKI resistance: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Astragaloside IV Co-Loaded Osimertinib Liposomes Alleviate EGFR-TKI Resistance in Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Article
- Non-small cell lung cancer after EGFR-TKI resistance: from drug resistance mechanisms to precision interventions.Frontiers in pharmacology · 2026Review
- The STAT3-ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer.Frontiers in oncology · 2026Article
- USP1-TRAF2 axis-regulated mortalin stability mediates chemoresistance by disrupting calcium transport in peripheral T-cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TKI resistance related genes in LUAD predict patient prognosis and tumor immune microenvironment with LHX2 as a hub gene.Discover oncology · 2025Article
- Circular RNA FCHO2 promotes airway remodeling in COPD via regulating nuclear translocation of PTBP1 to repress the splicing of GRN pre-mRNA.Cell death & disease · 2025Article
- Targeting RRM2 with dual-modal theranostic smart nanoresponder overcomes osimertinib resistance and triggers immune remodeling in NSCLC.Science advances · 2025Article
- Targeting Metabolic Vulnerabilities Reveals Hexokinase 2 as a Key Mediator of Resistance to Osimertinib in Non-Small Cell Lung Cancer Models.ACS pharmacology & translational science · 2025Article
- Drug tolerance and persistence to EGFR inhibitor treatment are mediated by an ILK-SFK-YAP signaling axis in lung adenocarcinoma.Oncogene · 2025Article
- TGFB2 Expression and Methylation Predict Overall Survival in Pancreatic Ductal Adenocarcinoma Patients.International journal of molecular sciences · 2025Article
- Strategies Beyond 3rd EGFR-TKI Acquired Resistance: Opportunities and Challenges.Cancer medicine · 2025Review
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osimertinib (AZD9291) has been widely used for the treatment of EGFR mutant non-small cell lung cancer. However, resistance to osimertinib is inevitable. In this study we elucidated the molecular mechanisms of resistance in osimertinib-resistant NCI-H1975/OSIR cells. We showed that NCI-H1975/OSIR cells underwent epithelial-mesenchymal transition (EMT), which conferred sensitivity to the GPX4 inhibitor 1S, 3R-RSL3 to induce ferroptotic cell death. The EMT occurrence resulted from osimertinib-induced upregulation of TGFβ2 that activated SMAD2. On the other hand, we revealed that NCI-H1975/OSIR cells were highly dependent on NF-κB pathway for survival, since treatment with the NF-κB pathway inhibitor BAY 11-7082 or genetic silence of p65 caused much greater cell death as compared with the parental NCI-H1975 cells. In NCI-H1975 cells, osimertinib activated NF-κB pathway, evidenced by the increased p65 nuclear translocation, which was abolished by knockdown of TGFβ2. In the cancer genome atlas lung adenocarcinoma data, TGFB2 transcript abundance significantly correlated with EMT-associated genes and NF-κB pathway. In addition, coexistence of EMT and activation of NF-κB pathway was observed in several NCI-H1975/OSIR clones. These findings shed new light on distinct roles of TGFβ2 in osimertinib-resistant cells and provide new strategies for treatment of this resistant status.
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