ArticleInvestigational new drugs2021
FGFR leads to sustained activation of STAT3 to mediate resistance to EGFR-TKIs treatment.
Article in Investigational new drugs, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- CSF1R inhibitors mitigate CDK4/6 inhibitor-induced immunosuppression to increase antitumor immunity in HR+/HER2- breast cancer.Oncogene · 2026Article
- Ascomycin enhances the antitumor activity of osimertinib in EGFR-TKI-resistant non-small cell lung cancer.Frontiers in oncology · 2026Article
- Article
- Leveraging Acquired EGFR-TKI-Resistant Models to Identify MUC16 as a Therapeutic Vulnerability in Lung Adenocarcinoma.Pharmaceuticals (Basel, Switzerland) · 2025Article
- A Pseudomonas aeruginosa quorum-sensing inducer controls lung permeability in establishing chronic infection via EGFR.Nature communications · 2025Article
- Traditional Chinese Medicines as Anticancer Agents for Non-Small Cell Lung Cancer with EGFR Mutations: A Review.Drug design, development and therapy · 2025Review
- STAT3-specific nanocarrier for shRNA/drug dual delivery and tumor synergistic therapy.Bioactive materials · 2024Article
- STAT3: Key targets of growth-promoting receptor positive breast cancer.Cancer cell international · 2024Review
- Sponge-derived alkaloid AP-7 as a sensitizer to cisplatin in the treatment of multidrug-resistant NSCLC via Chk1-dependent mechanisms.Frontiers in pharmacology · 2024Article
- Selumetinib overcomes gefitinib primary and acquired resistance by regulating MIG6/STAT3 in NSCLC.Archives of pharmacal research · 2023Article
- Identification of single nucleotide polymorphisms (SNPs) associated with chronic graft-versus-host disease in patients undergoing allogeneic hematopoietic cell transplantation.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2023Article
- Overcoming Acquired Drug Resistance to Cancer Therapies through Targeted STAT3 Inhibition.International journal of molecular sciences · 2023Review
- Twist1 as a target for prevention of cutaneous squamous cell carcinoma.Molecular carcinogenesis · 2023Article
- Tumor-associated macrophages mediate resistance of EGFR-TKIs in non-small cell lung cancer: mechanisms and prospects.Frontiers in immunology · 2023Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have led to great advances in the treatment of non-small cell lung cancer (NSCLC), but the emergence of drug resistance severely limits their clinical use. Thus, elucidation of the mechanism underlying resistance to EGFR-TKIs is of great importance. In our study, sustained activation of STAT3 was confirmed to be involved in resistance to EGFR-TKIs, and this resistance occurred regardless of exposure time, EGFR-TKIs type, and even cancer cell type. Mechanistically, the sustained activation of STAT3 was not related to gp130/JAK signalling pathway or HER2/EGFR heterodimer formation, while related to the expression and activation levels of STAT3. Furthermore, FGFR was shown to bind more strongly to STAT3 after gefitinib treatment, and the inhibition of FGFR reduced the phosphorylation of STAT3, thereby counteracting the effects of EGFR-TKIs and resulting in the synergistic inhibition of cancer cell proliferation. Taken together, the FGFR/STAT3 axis mediates the sustained activation of STAT3 upon EGFR-TKI treatment. This finding elucidates a new mechanism underlying drug resistance to EGFR-TKIs that the FGFR/STAT3 axis mediates the sustained activation of STAT3, providing theoretical support for considering the combination of TKIs and FGFR inhibitors in clinical cancer treatment.
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