Targeting lung cancer with clinically relevant EGFR mutations using anti-EGFR RNA aptamer.
EGFR resistance mutations
MT: Delivery Strategies
aptamers
biodistribution
molecular engineering
non-small cell lung cancer
oligonucleotides
targeted delivery
tumor cell-surface receptors
Journal
Molecular therapy. Nucleic acids
ISSN: 2162-2531
Titre abrégé: Mol Ther Nucleic Acids
Pays: United States
ID NLM: 101581621
Informations de publication
Date de publication:
12 Dec 2023
12 Dec 2023
Historique:
received:
01
05
2023
accepted:
29
09
2023
medline:
23
10
2023
pubmed:
23
10
2023
entrez:
23
10
2023
Statut:
epublish
Résumé
A significant fraction of non-small cell lung cancer (NSCLC) cases are due to oncogenic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). Anti-EGFR antibodies have shown limited clinical benefit for NSCLC, whereas tyrosine kinase inhibitors (TKIs) are effective, but resistance ultimately occurs. The current landscape suggests that alternative ligands that target wild-type and mutant EGFRs are desirable for targeted therapy or drug delivery development. Here we evaluate NSCLC targeting using an anti-EGFR aptamer (MinE07). We demonstrate that interaction sites of MinE07 overlap with clinically relevant antibodies targeting extracellular domain III and that MinE07 retains binding to EGFR harboring the most common oncogenic and resistance mutations. When MinE07 was linked to an anti-c-Met aptamer, the EGFR/c-Met bispecific aptamer (bsApt) showed superior labeling of NSCLC cells
Identifiants
pubmed: 37869258
doi: 10.1016/j.omtn.2023.102046
pii: S2162-2531(23)00264-0
pmc: PMC10589377
doi:
Types de publication
Journal Article
Langues
eng
Pagination
102046Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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