Document Type
Article
Publication Date
11-2024
Abstract
Non-small cell lung cancer (NSCLC) adenocarcinoma (LUAD) is a leading cause of death worldwide. Activating mutations in the tyrosine kinase domain of the oncogene epidermal growth factor receptor (EGFR) are responsible for ~10–50% of all LUAD cases. Although tyrosine kinase inhibitors (TKIs) have been effective in prolonging patient survival and quality of life, acquired resistance and disease progression are inevitable, presenting a clear unmet need for alternative or adjuvant therapeutics. Here we show that an anti-EGFR aptamer (EGFRapt) decreases viability and tumor growth of LUAD cell lines harboring the L858R ± T790M mutation in EGFR. Additionally, we elucidate the mechanism by which EGFRapt exerts these effects by monitoring cellular processes associated with kinase-dependent and kinase-independent mechanisms. Overall, these data establish that EGFRapt has direct anti-cancer activity in mutant EGFR positive LUAD via targetable mechanisms that are independent of existing approaches, and they provide a foundation for further development of nucleic acid-based therapies that target EGFR.
Recommended Citation
Thomas, B.J., Awan, S.Z., Joshi, T., Daniels, M.A., Porciani, D. and Burke, D.H., 2024. Anti-EGFR aptamer exhibits direct anti-cancer effects in NSCLC cells harboring EGFR L858R mutations. NPJ Precision Oncology, 8(1), p.271. https://doi.org/10.1038/s41698-024-00758-9
Comments
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