ArticleFrontiers in genetics2022
TROY Modulates Cancer Stem-Like Cell Properties and Gefitinib Resistance Through EMT Signaling in Non-Small Cell Lung Cancer.
Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Role of tumor necrosis factor receptor superfamily member 19 in cancer: Diverse functions and therapeutic potential (Review).Oncology letters · 2026Review
- Aberrantly High Expression of Steroid Receptor Coactivator-1 Drives Lung Cancer Growth and Metastasis by Enhancing Cancer Stemness.Biomolecules & therapeutics · 2025Article
- Construction and validation of an EGFR-related risk signature identifiedTranslational cancer research · 2025Article
- Epithelial-mesenchymal transition (EMT) and its role in acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) chemoresistance in non-small cell lung cancer (NSCLC).Cancer pathogenesis and therapy · 2025Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Targeted therapy has made breakthrough progress in the treatment of advanced non-small cell lung cancer (NSCLC) in the last 20 years. Despite that, acquired resistance of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is an urgent clinical problem. Our study established an acquired gefitinib-resistant cell line, which exhibited epithelial-mesenchymal transition (EMT) and stem cell-like properties. Transcriptional sequencing and bioinformatics analysis revealed that TROY was significantly increased in gefitinib-resistant cells. Gene set enrichment analysis (GSEA) showed EMT was the core enriched hallmark in the resistant cells. TROY siRNA interference could overcome the gefitinib resistance with the downregulated expression of EMT and CSC markers. In addition, immunohistochemistry indicated that TROY was overexpressed in tumor samples from patients who acquired resistance to first-generation EGFR-TKI without T790M mutation and the expression of TROY was associated with poor prognosis in LUAD. Here, we provided the potential role of TROY in the resistance of targeted therapy and a new strategy to overcome the acquired resistance to EGFR-TKI in NSCLC.
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