In vitro analysis of the molecular mechanisms of ursolic acid against ovarian cancer

被引：1

作者：

Zhang, Ru ^{[1
]}

Zhang, Zhaopeng ^{[2
]}

Xie, Lulu ^{[3
]}

Yu, Ziqing ^{[1
]}

Gao, Rui ^{[1
]}

Zhang, Zhi-Run ^{[1
]}

Zhang, Ying ^{[1
]}

Wei, Xuyang ^{[1
]}

Chen, Yang ^{[1
]}

Jiao, Sue ^{[1
]}

Gao, Yiren ^{[3
]}

Guo, Jun-Peng ^{[1
]}

机构：

[1] Changchun Univ Chinese Med, Sch Clin Med, Changchun, Peoples R China

[2] Changchun Univ Tradit Chinese Med, Sch Pharm, Changchun, Peoples R China

[3] Changchun Univ Tradit Chinese Med, Affiliated Hosp, Changchun, Peoples R China

来源：

BMC COMPLEMENTARY MEDICINE AND THERAPIES | 2025年 / 25卷 / 01期

关键词：

Ursolic acid; Anti-ovarian cancer; ERS; Autophagy; Apoptosis; ENDOPLASMIC-RETICULUM STRESS; AUTOPHAGY; TUMOR; CELLS; INHIBITION; ACTIVATION; INDUCTION; APOPTOSIS; BECLIN1; PROTEIN;

D O I：

10.1186/s12906-025-04808-y

中图分类号：

R [医药、卫生];

学科分类号：

10 ;

摘要：

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(eIF2 alpha), and The C/EBP Homologous Protein(CHOP) expression.In addition UA upregulates PERK, eIF2 alpha, 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.

引用

页数：12

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