医学分子生物学杂志 ›› 2025, Vol. 22 ›› Issue (1): 23-28.doi: 10.3870/j.issn.1672-8009.2025.01.004

• 论著 • 上一篇    下一篇

五味子酯乙靶向 PTGS1 抑制子宫内膜癌细胞增殖和上皮间质转化 #br#

  

  1. 陆军军医大学士官学校附属医院1预防保健科,2妇产科 石家庄市, 050041 3陆军军医大学士官学校战救医疗系 石家庄市, 050041
  • 出版日期:2025-01-31 发布日期:2025-02-28
  • 基金资助:
    河北省卫生健康委科研基金 (No. 20191730), 河北省 2022 年度医学科学研究课题 (No. 20221905)

Mechanism of Schisantherin B Inhibiting Proliferation of Uterine Corpus Endometrial Carcinoma Cells and Epithelial-mesenchymal Transition by Targeting PTGS1 #br#

  1. 1Department of Preventive Health Care,2 Department of Obstetrics and Gynecology, Affiliated Hospital of Non-Commissioned Officer School, Army Military Medical University, Shijiazhuang, 050041, China 3 Department of Combat Rescue Medicine, Military Medical University, Shijiazhuang, 050041, China
  • Online:2025-01-31 Published:2025-02-28

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摘要： 目的 分析五味子酯乙靶向前列腺素内过氧化物合酶 1 ( prostaglandin-endoperoxide synthase 1,PTGS1) 抑制子宫内膜癌 (uterine corpus endometrial carcinoma, UCEC) 细胞增殖和上皮间质转化 (epithelial-mesenchymal transition, EMT) 的机制。 方法 TargetNet 预测五味子酯乙的靶点 PTGS1, TCGA 数据库分析 UCEC 中高表达基因 PTGS1 与临床病理特征的关系。 设置对照组、 五味子酯乙组和 sh-PTGS1 组, 检测各组细胞生存率、 克隆细胞数和细胞 EMT 相关蛋白 ( E-cadherin、 Vimentin、 N-cadherin、 Snail) 表达情况。观察 PTGS1 对移植瘤体积、 重量, 和增殖指数 (Ki67) 表达的影响。 构建稳定过表达 PTGS1 的 Ishikawa 和HEC108 细胞, 检测五味子酯乙对过表达 PTGS1 的 Ishikawa 和 HEC108 细胞存活情况、 克隆细胞数和 EMT蛋白表达的影响。 结果 与对照组比较, sh-PTGS1 组和五味子酯乙组中细胞增殖和细胞克隆数以及PTGS1、 Vimentin、 N-cadherin、 Snail 表达明显下降, E-cadherin 表达明显上升 ( P< 0. 05); sh-PTGS1 组移植瘤模型中移植瘤组织体积、 质量和 Ki67 表达水平均明显降低 (P< 0. 05); PTGS1 过表达组细胞中 E-cadherin 明显下降, Vimentin、 N-cadherin、 Snail、 PTGS1 表达水平, Ishikawa 和 HEC108 细胞活性和克隆细胞数明显上升 (P< 0. 05)。 与五味子酯乙组比较, 五味子酯乙 + PTGS1 过表达组 E-cadherin 明显下降, Vimentin、 N-cadherin、 Snail、 PTGS1 明显上升 ( P < 0. 05)。 结论 五味子酯乙可能通过靶向 PTGS1, 下调PTGS1 表达水平, 抑制 UCEC 增殖和 EMT 发生。

关键词: 五味子酯乙, 子宫内膜癌, 细胞增殖, 上皮间质转化, 前列腺素内过氧化物合酶 1

Abstract: Objective To analyze the mechanism of Schisantherin B inhibiting the proliferationof uterine corpus endometrial carcinoma ( UCEC ) cells and epithelial-mesenchymal transition( EMT ) by targeting prostaglandin-endoperoxide synthase 1 ( PTGS1 ) . Methods The target( PTGS1) of Schisantherin B was predicted by TargetNet. The relationship between the expression ofPTGS1 and the clinicopathological characteristics of UCEC was analyzed by TCGA database. Thecontrol group, Schisantherin B group and sh-PTGS1 group were set up. The survival and colony formation abilities of cells, and the expression levels of EMT associated proteins were detected. Theeffect of PTGS1 on volume and weight of xenograft tumors, and the level of proliferation index(Ki67) were observed. Ishikawa and HEC108 cell lines with stable overexpression of PTGS1 wereconstructed. The effect of Schisantherin B on survival, colony formation abilities, and expressionlevels of EMT proteins of Ishikawa and HEC108 cells with PTGS1 overexpression were detected. Results Compared with those in the control group, the proliferation and numbers of cell colonies, and the expression levels of PTGS1, Vimentin, N-cadherin and Snail in the sh-PTGS1 group and the Schisantherin B group were significantly decreased, the expression level of E-cadherin in the above two groups was significantly increased; the volume and weight of xenograft tumor tissues,and the expression level of Ki67 in the sh-PTGS1 group were significantly decreased ( P < 0. 05). However, the expression level of E-cadherin was significantly decreased in the PTGS1 overexpression group, the expression levels of PTGS1, Vimentin, N-cadherin, Snail, and the cell viabilities, and number of cell colonies of Ishikawa and HEC108 cells were significantly increased when compared with those in the control group (P< 0. 05). In addition, when compared with those in theSchisantherin B group, the expression level of E-cadherin was significantly decreased in the Schisandrin B + PTGS1 overexpression group, while the expression levels of PTGS1, Vimentin,N-cadherin, Snail were significantly increased (P < 0. 05). Conclusion Schisantherin B may inhibit the proliferation and EMT of UCEC cells by down-regulating PTGS1.

Key words: Schisantherin B, uterine corpus endometrial carcinoma, cell proliferation, epithelial mesenchymal transition, prostaglandin-endoperoxide synthase 1

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