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GLMP promotes EGFR-TKI resistance by activating autophagy and RhoA pathway in non-small cell lung cancer

GSE298111 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/12/10 Platform GPL24676
Summary
Here, we report that the EGFR-TKI resistance mechanism is mediated by lysosome-related regulation. We established an osimertinib-resistant cell line, designated PC9OR, derived from the parental PC9 cells. The overexpression of glycosylated lysosomal membrane protein (GLMP) in PC9OR promotes resistance to Osimertinib. Mechanistically, GLMP could regulate the ubiquitination of RhoA and promote resistance by activating the epithelial-mesenchymal transition (EMT). Our findings provide a potential therapeutic strategy to overcome resistance to EGFR-TKIs.
Published in
GLMP promotes EGFR-TKI resistance by activating autophagy and RhoA pathway in non-small cell lung cancer
Liang X, Xu J, Shu S et al. · NPJ precision oncology 2025 · PMID 41298761 · doi:10.1038/s41698-025-01135-w
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Also filed as BioProject PRJNA1268374 and SRA study SRP588451. Searching any of these in the dataset finder brings you back here.

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