ArticleJournal of experimental & clinical cancer research : CR2026
Icaritin eliminates tumor-associated macrophages via STX16-dependent extracellular vesicle delivery of autophagosomes from hepatocellular carcinoma cells.
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
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11 authors.
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Abstract
backgroundTo elucidate the mechanism by which icaritin—a novel agent for hepatocellular carcinoma (HCC)—remodels the tumor microenvironment (TME) by inhibiting HCC cell metabolism-mediated M2 polarization of tumor-associated macrophages (TAMs).
methodsIntegrative approaches spanning in vitro Transwell cocultures, RNA-seq, LC3-based autophagy tracing, STX16 gene edition, and orthotopic xenografts mechanistically dissected the affective and mechanism of icaritin in remodeling TME.
resultsOur results indicate that icaritin transcriptionally suppresses ALDOB in HCC cells to reduce lactate production. Consequently, the lactylation of histone H3 at lysine 9 and lysine 18 (H3K9/H3K18la) on the STX16 promoter is diminished, thereby ablating STX16 transcription. STX16 deficiency blocks autophagolysosome biogenesis, leading to the accumulation of autophagosomes in HCC cells. These autophagosomes are subsequently delivered to macrophages via extracellular vesicle (EVs) and then triggers autophagic cell death and p62-guided STAT3 destruction within the macrophages, thereby eliminating M2 TAMs and reprograming the tumor immune microenvironment. In vivo validation confirmed icaritin suppressed tumor growth and M2 macrophage infiltration via the ALDOB/STX16/autophagy/STAT3 axis.
conclusionThese results indicate that by orchestrating a novel "metabolism-epigenetics-autophagy-EVs" cascade to eliminate TAMs, icaritin targets ALDOB, STX16, and STAT3, revealing key nodes for therapeutic intervention.
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