ArticleScientific reports2025
The novel amino-artemisinin derivative WHN-11 disrupts mitochondria and protein homeostasis, and induces autophagy and apoptosis in cancer cells.
Article in Scientific reports, 2025. 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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Abstract
Semi-synthetic derivatives of artemisinin exhibit anti-cancer activity in vitro and in vivo in addition to anti-malarial activity. Here, we report the anti-cancer and anti-cancer stem cell potential of novel C-10 substituted amino-artemisinin derivatives. Of these, the 4'-trifluoromethylarylurea piperazinyl derivative WHN-11 demonstrated cytotoxic activity at high nanomolar concentrations across a range of cancer cell lines. WHN-11 reduced short- and long-term survival of triple-negative breast cancer (TNBC) cells, a highly aggressive breast cancer subtype that currently lacks standardized targeted treatments. Mechanistically, WHN-11 induced a stress response and increased proteasome-mediated turnover of ubiquitinated proteins. WHN-11 promoted mitochondrial depolarization and fission, suppressing the expression of anti-apoptotic B-cell lymphoma extra-large (Bcl-xL) protein and ATP synthesis, thereby decreasing cellular energy production, and inducing apoptosis. WHN-11 treatment also increased autophagosomes, acidic vesicular organelles and lipid droplets. Activation or inhibition of autophagy synergized with the activity of WHN-11 in promoting cellular toxicity, as did increasing cellular dependence on oxidative phosphorylation. Unexpectedly, the effects of WHN-11 appear independent of substantial reactive oxygen species (ROS) production. Taken together, these data suggest that amino-artemisinins related to WHN-11 are promising candidates for anti-TNBC therapies targeting the mitochondria alone or in combination with autophagy modulators.
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