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• W4383112323 abstract "Artemisinin, originally used for its antimalarial activity, has received much attention in recent years for cancer therapy. The anticancer mechanisms of artemisinin are complicated and debatable. Challenges in the delivery of artemisinin also persist because the anticancer effect of artemisinin alone is often not satisfactory when used with traditional nanocarriers. We herein report the mitochondrial delivery of artemisinin with extremely high anticancer capacity. The action mode of artemisinin in the mitochondria of cancer cells includes heme-participating and oxygen-independent conversion of artemisinin into a carbon-centered radical, which is partly converted into ROS in the presence of molecular oxygen. We reveal that artemisinin alone in the mitochondria can induce strong cancer cell apoptosis. In addition, due to the weak inhibition of GPX4 activity by artemisinin, weak ferroptosis is also observed. We further discover that GPX4 activity in MCF-7 cells is greatly inhibited by RSL3 to synergistically enhance the anticancer capacity of artemisinin via enhancing ferroptosis. The synergistic anticancer activity of artemisinin and RSL3 in the mitochondria not only improves cancer cell-killing ability, but also inhibits the re-proliferation of residual cancer cells. This study provides a new insight into developing highly efficient and practical artemisinin nanomedicines for cancer therapy." @default.
• W4383112323 created "2023-07-05" @default.
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• W4383112323 date "2023-01-01" @default.
• W4383112323 modified "2023-10-14" @default.
• W4383112323 title "GPX4 inhibition synergistically boosts mitochondria targeting nanoartemisinin-induced apoptosis/ferroptosis combination cancer therapy" @default.
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• W4383112323 doi "https://doi.org/10.1039/d3bm00601h" @default.
• W4383112323 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37439624" @default.
• W4383112323 hasPublicationYear "2023" @default.
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