ArticleCancer cell international2025
Icariin-curcumol inhibits histone H3K18 lactylation and FOXM1 expression to enhance the sensitivity of prostate cancer cells to docetaxel.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Rhaponticin Blocks Glycolysis-Mediated Histone Lactylation to Suppress Tongue Squamous Cell Carcinoma via HIF-1α Activity Inhibition.The Kaohsiung journal of medical sciences · 2026Article
- Review
- Protein lactylation: a metabolic signal driving cancer therapy resistance.Cell death discovery · 2026Review
- Lactylation in urological malignancies: emerging mechanisms and therapeutic direction.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
13 authors.
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Abstract
backgroundHistone lactylation has emerged as an epigenetic driver of tumor chemoresistance. Our prior work identified the phytochemical combination icariin-curcumol (Ica-Cur) as a potential therapeutic agent against docetaxel (DTX)-resistant prostate cancer (PCa). This study aimed to investigate the mechanistic link between histone lactylation and DTX resistance in PCa, and evaluates Ica-Cur's regulatory role in this process.
methodsDTX-resistant LNCaP/R cells were generated from parental LNCaP PCa cells. Xenograft models were established in BALB/c nude mice using both cell lines. Interventions included pharmacological modulation of glycolysis (sodium lactate [Nala], a glycolysis activator and 2-deoxy-D-glucose [2-DG], a glycolysis inhibitor) and genetic silencing of forkhead box M1 (FOXM1) via lentiviral constructs (sh-FOXM1). The enrichment of histone H3K18 lactylation (H3K18la) at the FOXM1 promoter was validated. Tumor growth, lactate levels, lactate dehydrogenase (LDH) activity, proliferation, and apoptosis were systematically analyzed.
resultsResistant LNCaP/R models exhibited significant upregulation of H3K18la and FOXM1 compared to controls. Nala increased lactate production, enhanced H3K18la deposition, and stimulated proliferation while suppressing apoptosis. Conversely, 2-DG reduced H3K18la deposition and inhibited proliferation. FOXM1 expression was directly regulated by H3K18la, with sh-FOXM1 reducing LDH activity, inhibiting proliferation, and inducing apoptosis. Ica-Cur restored DTX sensitivity by suppressing H3K18la and FOXM1 expression.
conclusionThese findings identify H3K18la-mediated FOXM1 activation as a novel mechanism underlying DTX resistance in PCa. Ica-Cur may represent a promising therapeutic agent by targeting lactylation-dependent epigenetic regulation and FOXM1-driven transcriptional activity, supporting its clinical potential for overcoming chemoresistance.
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