ArticleBMC complementary medicine and therapies2025
In vitro analysis of the molecular mechanisms of ursolic acid against ovarian cancer.
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ursolic acid in cancer therapy: a review of signaling pathways and apoptotic mechanisms.Molecular biology reports · 2026Review
- Ursolic acid as a multifunctional anticancer agent with insights into molecular mechanisms therapeutic potential and formulation strategies.Discover oncology · 2026Review
- A Combination of Xanthohumol and Ursolic Acid in the Diet Leads to Synergistic Inhibition of Prostate Cancer Progression.Molecular carcinogenesis · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Current Research on the Control Mechanisms of Cell Survival and Proliferation as Potential Interaction Sites with Pentacyclic Triterpenoids in Ovarian Cancer.International journal of molecular sciences · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
Ovarian cancer is one of most common gynaecologic malignancy and ranks third in cancer-related deaths among women. Ursolic acid (UA) is a pharmacologically active pentacyclic triterpenoid isolated from a large variety of vegetables, fruits and many traditional medicinal plants. However, the mechanism of action of UA in inhibiting the proliferation of ovarian cancer cells remains unclear. Consequently, this experiment was designed to elucidate the mechanism of action of UA in inhibiting the proliferation of ovarian cancer cells in greater detail.The results indicated that UA was capable of effectively inhibiting the proliferation, migration, and colony formation of ovarian cancer cells.UA was observed to up-regulate Bcl-2-associated X protein(BAX)and cysteinyl aspartate specific proteinase 3 (Caspase3) expression and down-regulating B-cell lymphoma-2(Bcl-2) expression.Meanwhile, UA up-regulated Sequestosome 1(p62)expression and down-regulated coiled-coil, moesin-like BCL2-interacting protein(Becline1), microtubule-associated proteins light chain 3(LC3), Phosphoinositide 3-Kinase(PI3K), andProtein Kinase B( AKT) expression, thus effectively inhibiting autophagy in ovarian cancer cells.Furthermore, UA upregulated pancreatic ER kinase (PKR)-like ER kinase (PERK), eukaryotic translation initiation factor 2 A(eIF2α), and The C/EBP Homologous Protein(CHOP) expression.In addition UA upregulates PERK, eIF2α, and CHOP expression and effectively promotes endoplasmic reticulum stress(ERS).In conclusion, UA can inhibit ovarian cancer cell proliferation, migration, colony formation, and may inhibit tumor cell autophagy by promoting tumor cell ERS, and ultimately promote ovarian cancer cell apoptosis.
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