ArticleBMC biotechnology2026
Mitochondria-targeted CORM-401 nanoparticles inhibit A549 cells by triggering cuproptosis.
Article in BMC biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Engineering cuproptosis with nanomedicine: Design, combination therapy, and translation in cancer.Materials today. Bio · 2026Review
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Abstract
objectiveIn this study, mitochondrial-targeted nanoparticles containing CORM-401 were designed by using TPP and HA (named as CORM-TPP@HA). The effects of these nanoparticles on cuproptosis in A549 cells were observed to confirm their function.
methodsFirst, CORM-TPP micelles were formed by using CORM-401 and TPP-SH. Then, the micelles were encapsulated with HA to form nanoparticles (CORM-TPP@HA). The morphology, size distribution, stability, and release of CO from nanoparticles were analyzed to confirm their characterization. Meanwhile, the cellular uptake of nanoparticles was observed using a confocal microscope. The effects of the nanoparticles on cell viability, mitochondrial ROS, intracellular copper, and cuproptosis-related proteins in A549 cells were measured. Additionally, the impacts of nanoparticles on tumor growth and cuproptosis-related factors in tumor tissue were measured in vivo.
resultsThe designed nanoparticles maintained stable formation, effectively preventing premature CO release from CORM-401. Furthermore, the nanoparticles were able to be taken up by A549 cells. Moreover, treatment with the designed nanoparticles induced cuproptosis by increasing mitochondrial ROS, intracellular copper, and cuproptosis-related proteins in A549 cells. In line with the in vitro results, treatment with nanoparticles suppressed tumor growth and elevated the cuproptosis-related proteins in tumor tissues.
conclusionThe synthesized CORM-TPP@HA nanoparticles suppressed A549 cells via regulating mitochondrial cuproptosis, providing a signaling mechanism of CO in NSCLC treatment.
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