ArticleJournal of cellular and molecular medicine2026
FoxO3a-Mediated Modulation of PD-L1 Expression and Inhibition by Dihydroartemisinin in Triple-Negative Breast Cancer.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- FoxO3a-Mediated Modulation of PD-L1 Expression and Inhibition by Dihydroartemisinin in Triple-Negative Breast Cancer.Journal of cellular and molecular medicine · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Tumour immunotherapy targeting PD-1/PD-L1 shows promise, but the regulatory mechanisms of PD-L1 and its small-molecule modulators remain unclear. This study investigated FoxO3a-mediated PD-L1 regulation and the PD-L1-inhibitory role of dihydroartemisinin (DA) in triple-negative breast cancer (TNBC). FoxO3a overexpression significantly increased PD-L1 expression and impaired T cell-mediated cytotoxicity, while knockdown exerted opposite effects in TNBC cells. Promoter motif analysis and dual-luciferase assays revealed FoxO3a binding to the s155 site on the PD-L1 promoter in MDA-MB-231 cells; mutation of s155 abolished this interaction. ChIP-PCR confirmed FoxO3a binding to the PD-L1 promoter at s155. Furthermore, DA, a clinical antimalarial, reduced PD-L1 and FoxO3a levels, sensitising TNBC cells to T cell killing in TNBC cells. Mechanistically, DA enhanced IRE1/IKK phosphorylation, promoting FoxO3a Ser644 phosphorylation and ubiquitination. Crucially, s155 was required for DA-induced PD-L1 suppression in MDA-MB-231 cells. These findings demonstrate PD-L1 as a direct transcriptional target of FoxO3a and identify DA as a potential TNBC therapeutic targeting the IRE1/IKK/FoxO3a/PD-L1 axis.
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Registered trials
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