ArticleClinical and translational medicine2026
miR-941 in extracellular vesicles confers anlotinib resistance via Keap1/Nrf2 axis and represents a therapeutic target in non-small cell lung cancer.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAnlotinib is a multitargeted tyrosine kinase inhibitor for the treatment of advanced non-small cell lung cancer (NSCLC), though its therapeutic efficacy is constrained by acquired resistance. Although elevated extracellular vesicle (EV)-derived miR-941 correlates with anlotinib resistance, its functional role remains unexplored. Here, we provide evidence that EV-delivered miR-941 mediates this resistant phenotype.
methodsFunctional experiments (gain- and loss-of-function) in A549 and H1299 cells assessed viability, apoptosis and migration. The miR-941/Keap1 interaction was validated using dual-luciferase assays. In vivo resistance was evaluated using wild-type and Keap1 3'UTR-mutant xenograft models. Clinical relevance and survival outcomes were analysed in tumour tissues from anlotinib-treated patients.
resultsEV-derived miR-941 was significantly upregulated in anlotinib-resistant patients. Mechanistically, miR-941 directly targeted the Keap1 3'UTR, suppressing Keap1 protein and activating the Nrf2 signalling pathway. This axis inhibited apoptosis, upregulated anti-apoptotic proteins (Bcl-2, Mcl-1), and promoted malignant phenotypes in vitro. Crucially, in vivo anlotinib resistance induced by miR-941 overexpression was completely abrogated by mutating the Keap1 binding site. Clinical samples confirmed elevated miR-941 and a molecular signature consistent with Keap1 downregulation and Nrf2 activation in resistant tumours. Furthermore, high expression of miR-941 was strongly associated with shorter progression-free survival and overall survival.
conclusionIn this study, we identified EV-derived miR-941 as a key driver of anlotinib resistance via the Keap1/Nrf2 pathway. It represents a promising non-invasive predictive biomarker and serves as a candidate therapy target for overcoming drug-resistant NSCLC. KEY POINTS: EV-derived miR-941 as a key driver of anlotinib resistance via the Keap1/Nrf2 pathway represent a promising non-invasive predictive biomarker and a potential therapeutic target for overcoming resistance in NSCLC.
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