Journal of Medical Molecular Biology ›› 2025, Vol. 22 ›› Issue (1): 23-28.doi: 10.3870/j.issn.1672-8009.2025.01.004

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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

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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