文献类型：期刊文献

英文题名：Paeonol inhibits the progression of endometrial cancer by affecting TRIM26-mediated LDHA ubiquitination modification

作者：Chen, Xu[1];Liu, Jianxing[2];Liang, Yongrui[1];Gong, Zihan[3,4]

第一作者：陈霞;陈欣;陈鑫

通信作者：Gong, ZH[1]

机构：[1]Gansu Univ Chinese Med, Inst Basic Med Sci, Lanzhou 730000, Peoples R China;[2]Shandong Second Med Univ, Inst Basic Med Sci, Weifang 261042, Peoples R China;[3]Ningxia Hui Autonomous Reg Acad Tradit Chinese Med, Ningxia Hui Autonomous Reg Hosp Tradit Chinese Med, Yinchuan 750021, Peoples R China;[4]Ningxia Med Univ, Affiliated Autonomous Reg Tradit Chinese Med Hosp, 114 Beijing West Rd, Yinchuan 750021, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Ningxia Med Univ, Affiliated Autonomous Reg Tradit Chinese Med Hosp, 114 Beijing West Rd, Yinchuan 750021, Peoples R China.

年份：2026

卷号：100

外文期刊名：TISSUE & CELL

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001693214300001)】；

基金：This study was supported by the Natural Science Foundation of Ningxia (2024AAC03727) and the Scientific Research Project of the Health and Wellness System of Ningxia Hui Autonomous Region (2024-

语种：英文

外文关键词：Paeonol; Endometrial cancer; Tripartite motif protein 26; Lactate dehydrogenase A; Ubiquitination

摘要：Endometrial cancer (EC) is a common gynecological malignancy characterized by abnormal glucose metabolism. Paeonol (Pae), a natural phenolic compound derived from traditional Chinese medicine, exhibits broad-spectrum antitumor activity. However, its role in modulating glycolysis and the underlying molecular mechanisms in EC remain poorly understood. The effects on EC cell viability (CCK-8), proliferation (EdU), apoptosis (flow cytometry), invasion (transwell), migration (wound healing), and tube formation rate were assessed. Glycolytic parameters were measured using corresponding commercial kits. Protein and mRNA expression levels were determined by Western blotting and RT-qPCR. The interaction between tripartite motif protein 26 (TRIM26) and lactate dehydrogenase A (LDHA) was investigated through co-immunoprecipitation (Co-IP), cycloheximide (CHX) chase, and ubiquitination assays. A xenograft model was established to examine the in vivo efficacy of Pae. Pae inhibited proliferation, metastasis, tube formation, and glycolysis of EC cells, and induced apoptosis. Pae suppressed EC malignant behaviors by downregulating LDHA expression. TRIM26 promoted ubiquitinationmediated degradation of LDHA. Overexpression of LDHA reversed the tumor-suppressive effects of TRIM26 overexpression in EC cells. TRIM26 knockdown attenuated the antitumor effects of Pae. In vivo experiments demonstrated that Pae inhibited tumor growth and regulated TRIM26/LDHA expression. Pae was found to promote TRIM26 expression, which in turn enhanced TRIM26-mediated ubiquitination and degradation of LDHA, thereby contributing to glycolysis inhibition and suppression of EC progression. These results suggested that Pae might exert its effects by modulating the TRIM26/LDHA axis and supported its potential therapeutic value in EC.