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Icariside II inhibits Epithelial-Mesenchymal transition in metastatic osteosarcoma by antagonizing the miR-194/215 cluster via PGK1

文献类型： 外文期刊

作者： Hu, Jianping 1 ; Chen, Jinhu 1 ; Zhao, Caili 1 ; Yu, Pei 1 ; Xu, Wenjun 1 ; Yin, Yong 1 ; Yang, Lei 1 ; Zhang, Zhenzhen 2 ; Kong, Lingyi 1 ; Zhang, Chao 1 ;

作者机构： 1.China Pharmaceut Univ, Sch Tradit Chinese Pharm, State Key Lab Nat Med, Jiangsu Key Lab Bioact Nat Prod Res, Nanjing 210009, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing 210014, Peoples R China

3.GuoTai Taizhou Ctr Technol Innovat Vet Biol, Taizhou 225300, Peoples R China

关键词： Icariside II; PGK1; miR-194/215 cluster; Metastatic osteosarcoma; EMT; Chemokines

期刊名称：BIOCHEMICAL PHARMACOLOGY （ 影响因子：5.6； 五年影响因子：5.7 ）

ISSN： 0006-2952

年卷期： 2025 年 236 卷

页码：

收录情况： SCI

摘要： Osteosarcoma, the most prevalent malignant bone tumor in adolescents, is characterized by its aggressiveness and tendency to metastasize. Despite the advancements in treatment that have improved survival rates for localized cases, metastatic osteosarcoma remains challenging to treat due to the limited efficacy of current therapies and the severe side effects of chemotherapy. Epithelial-mesenchymal transition (EMT) is a key factor in osteosarcoma metastasis, and the miR-194/215 cluster, which is upregulated in osteosarcoma, promotes this process. This study sought to investigate natural compounds that could counteract the miR-194/215 cluster's effects and inhibit osteosarcoma metastasis. By analyzing miRNA databases and clinical data, a signature gene set for the miR-194/215 cluster was established, and the LINCS database was screened to find natural compounds with antagonistic effects. Icariside II, an active component of Epimedium, was identified as a potential inhibitor and was shown to reduce the migration and invasion of osteosarcoma cells in vitro and lung metastasis in vivo. The study utilized various techniques, including Gene Set Enrichment Analysis (GSEA), Drug Affinity Responsive Target Stability (DARTS), Cellular Thermal Shift Assay (CETSA), molecular docking, and enzyme activity assays, to identify phosphoglycerate kinase 1 (PGK1) as the target protein of Icariside II. It was found that Icariside II competitively inhibits PGK1 by binding to its ADP binding pocket, reducing its activity and thus antagonizing the miR-194/215 cluster's promotion of EMT in metastatic osteosarcoma. The results suggest that Icariside II could be a promising therapeutic agent for metastatic osteosarcoma, providing new targets and strategies for clinical treatment.

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