ArticleChinese medicine2025
Triptolide targets PPP2CA/ITGA5 axis to suppress lactate-driven ovarian cancer progression.
Article in Chinese medicine, 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.
- Integrin α5β1 in pancreatic ductal adenocarcinoma: Tumour‒stroma crosstalk, hypoxia and therapeutic targeting.Clinical and translational medicine · 2026Review
- The synergistic applications of organoids and exosomes in disease modeling and disease treatment.Molecular biology reports · 2026Review
- Lactylation: a metabolic-epigenetic bridge in diabetic kidney disease and a therapeutic target for TCM.Chinese medicine · 2026Review
- Natural compounds targeting glycolysis and TME in ovarian cancer: from metabolic crosstalk to therapeutic potential.Frontiers in pharmacology · 2026Review
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9 authors.
Funding
Abstract
backgroundTriptolide, the active compound of Tripterygium wilfordii, exhibits broad anti-tumor activity. This study explores PPP2CA dysregulation in ovarian cancer (OC) progression via lactate production and evaluates Triptolide's potential to regulate this process.
methodsWe used patient-derived xenograft (PDX) models, cell proliferation, and migration assays to assess lactate's impact on OC progression. CRISPR-Cas9 was applied to knock out PPP2CA, examining its effect on lactate production and tumor progression. RNA-seq analyzed transcriptomic changes post-PPP2CA knockout. The PPP2CA-ITGA5 axis was validated using xenografts, immunofluorescence, immunohistochemistry staining and western blot. Exosome isolation and co-culture experiments with tumor cells and human peritoneal mesothelial cells (HPMCs) investigated ITGA5's role in migration. Finally, patient-derived organoids, xenograft tumor model, and lactate assays assessed Triptolide's reversal effect on PPP2CA dysregulation-driven OC progression.
resultsWe found that PPP2CA dysregulation significantly promotes OC proliferation, migration, and tumorigenesis by enhancing YAP nuclear translocation and upregulating ITGA5/ITGB1. PPP2CA dysregulation led to ITGA5 upregulation, where ITGA5, as part of the integrin α5β1 heterodimer, plays a key role in driving OC migration. Exosomal ITGA5 facilitates OC metastasis to the HPMCs. Triptolide effectively inhibited patient-derived organoid growth and reduced lactate production in OC cells. By suppressing ITGA5, Triptolide reversed cancer progression and restored tumor-suppressive effects in a PPP2CA-knockout xenograft model.
conclusionOur study reveals that Triptolide effectively inhibits OC progression by targeting the PPP2CA-ITGA5 axis, mitigating lactate-driven metabolic reprogramming.
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