ArticleJournal of nanobiotechnology2025
Bionic gene delivery system activates tumor autophagy and immunosuppressive niche to sensitize anti-PD-1 treatment against STK11-mutated lung adenocarcinoma.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Review
- Nanomaterial-driven spatiotemporal autophagy modulation: The dual-edged sword in precision cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Integration of immunogenic cell death in the treatment landscape of non-small cell lung cancer: harnessing the power of the immune system.Cell death discovery · 2026Review
- PTC124 promotes mutation site-dependent readthrough of STK11 nonsense mutations and restores tumor suppressor function.BBA advances · 2026Article
- Engineering the Future: Strategic Advances in Extracellular Vesicle-Mediated Drug Delivery Systems.International journal of nanomedicine · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
Clinical data have shown that Serine/Threonine Kinase 11 (STK11) mutation may be associated with an immunosuppressive tumor microenvironment (ITEM) and poor prognosis and failure of anti-PD-1 (αPD1) treatment in non-small cell lung cancer (NSCLC). To explore the potential of restoring STK11 protein in immunotherapy, a bionic gene delivery system was prepared by coating the STK11-encoded DNA-cationic polymer complex core with the tumor cell membrane, termed STK11@PPCM. STK11@PPCM could specifically bind with NSCLC cells and achieve precise delivery of STK11-encoded DNA. The released DNA effectively restored the STK11 protein expression, consequently reactivating autophagy and immunogenic cell death (ICD) in cancer cells. The liberated damage-associated molecular patterns (DAMPs) and autophagosome induced dendritic cells (DCs) maturation, which in turn enhanced CD8 + T cell infiltration, M1 macrophage polarization, and proinflammatory factor expression, thereby reversing the ITEM. Moreover, STK11@PPCM was also found to improve the sensitivity of cancer cells to αPD1 by increasing the expression of PD-L1, which was confirmed in STK11-mutated NSCLC cell xenografted mouse models, constructed by CRISPR-Cas9 knockout technology. This work demonstrated for the first time that restoration of functional STK11 can effectively reverse ITME and boost αPD1 efficacy in NSCLC, offering a new therapeutic approach for STK11-mutated lung adenocarcinoma in clinic.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.