ArticleJournal of nanobiotechnology2026
Biomimetic β-lapachone and hemin nanoassembly for intracellular oxidation cascade amplified ferroptosis in hepatocellular carcinoma therapy.
Article in Journal of nanobiotechnology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Targeting the NR3C1-ACSL4 Axis Triggers Ferroptosis to Overcome Radioresistance in Prostate Cancer.Cancer science · 2026Article
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14 authors.
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Abstract
Ferroptosis represents one of important no-apoptotic programmed cell death with over accumulation of iron- and reactive oxygen species (ROS). While its key role and trials for cancer therapy, achieving precise and potent induction ferroptosis in cancer cells with massive amplification of cellular lipid peroxidation and iron overloading, remains a significant hurdle. Herein, we developed a biomimetic red blood cell membranes (RBCM) camouflaged β-lapachone (Lap) and hemin nanoassembly (LHNPs@RBCM) as ferroptosis inducer for hepatocellular carcinoma (HCC) therapy. The RBCM endowed the nanoassembly with prolonged systemic circulation and improved tumor accumulation. After endocytosis of LHNPs@RBCM by cancer cells, the cancer-specific overexpressed NAD(P)H: quinone oxidoreductase (NQO1) converted the released Lap to ROS (e.g. O
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