ArticleRedox biology2026
Cooperative inhibition of mTORC1 disrupts iron-redox homeostasis and triggers ferritinophagy-dependent ferroptosis in hepatocellular carcinoma.
Article in Redox biology, 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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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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14 authors.
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Abstract
Hepatocellular carcinoma (HCC) remains a leading cause of cancer mortality, and the clinical utility of β-lapachone (β-Lap) is limited by dose-dependent toxicity. Here, we identify cryptotanshinone (CPT), a bioactive compound derived from Salvia miltiorrhiza, as a synergistic partner that enables dose reduction while enhancing antitumor efficacy. Integrated transcriptomic profiling, biochemical analyses, target engagement assays, and in vivo validation support that β-Lap and CPT cooperatively induce ferroptosis through disruption of iron-redox homeostasis. Mechanistically, β-Lap and CPT engage Raptor and mTOR, respectively, in vitro, supporting a model wherein their cooperative action leads to dual suppression of mTORC1 signaling. mTORC1 inhibition activates NCOA4-mediated ferritinophagy, promoting ferritin degradation and expansion of the labile Fe
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