ArticleCancers2026
Dihydroartemisinin Suppresses Hepatocellular Carcinoma Progression by Acting on KIF11 with PI3K/Akt Modulation.
Article in Cancers, 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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Authors and funding
3 authors.
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Abstract
BACKGROUND/
objectivesHepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with limited effective therapies. Dihydroartemisinin (DHA), a derivative of artemisinin, exhibits potent antitumor activity, but its molecular mechanisms in HCC are unclear. Here, we identified kinesin family member 11 (KIF11) as a critical effector of DHA.
methodsBioinformatic analyses revealed that KIF11 is significantly upregulated in HCC and associated with poor prognosis, and gene expression profiling suggested its oncogenic role via the PI3K/Akt pathway. Functional studies demonstrated that DHA inhibits HCC cell proliferation, migration, invasion, and colony formation, while inducing apoptosis. Xenograft models of nude mice were established for validation.
resultsDHA downregulated KIF11 and epithelial-mesenchymal transition markers, whereas KIF11 overexpression attenuated DHA's inhibitory effects; the inhibition of PI3K restored DHA sensitivity in KIF11-overexpressing cells. In vivo, DHA markedly suppressed tumor growth and malignancy in xenograft models, consistent with modulation of KIF11 and EMT-related proteins.
conclusionsDHA exerts antitumor effects in HCC by acting via KIF11 and PI3K/Akt modulation, providing a potential therapeutic strategy.
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