基础医学与临床 ›› 2025, Vol. 45 ›› Issue (12): 1565-1571.doi: 10.16352/j.issn.1001-6325.2025.12.1565

• 研究论文 • 上一篇    下一篇

miR-132-3p通过靶向调控SIRT1/NF-κB通路影响滋养层细胞上皮-间质转化

郭书焕, 高亚丽, 陈静鸽*   

  1. 郑州市妇幼保健院 妇产科,河南 郑州 450012
  • 收稿日期:2025-01-10 修回日期:2025-03-25 出版日期:2025-12-05 发布日期:2025-11-25
  • 通讯作者: *22204968@qq.com
  • 基金资助:
    河南省医学科技攻关计划联合共建项目(LHGJ20220873)

Effect of miR-132-3p on epithelial-mesenchymal transition of trophoblast cells by targeting the SIRT1/NF-κB pathway

GUO Shuhuan, GAO Yali, CHEN Jingge*   

  1. Department of Obstetrics and Gynecology, Women & Infants Hospital of Zhengzhou, Zhengzhou 450012, China
  • Received:2025-01-10 Revised:2025-03-25 Online:2025-12-05 Published:2025-11-25
  • Contact: *22204968@qq.com

摘要: 目的 探讨miR-132-3p靶向调控SIRT1/NF-κB通路对滋养层细胞上皮-间质转化(EMT)的影响。方法 收集于郑州市妇幼保健院行剖宫产术的37例子痫前期(PE)患者及同期行剖宫产术的37名正常孕妇的胎盘组织分别作为研究组和对照组,RT-qPCR检测组织中miR-132-3p、SIRT1 mRNA表达水平;取对数增殖期的HTR-8/SVneo细胞分为抑制剂阴性组、miR-132-3p抑制剂组、模拟物阴性组、miR-132-3p过表达组、miR-132-3p抑制剂+干扰阴性组、miR-132-3p抑制剂+干扰SIRT1组,并以未转染的HTR-8/SVneo细胞为空白组,CCK-8、Transwell实验、划痕实验及RT-qPCR检测HTR-8/SVneo细胞增殖、侵袭、迁移及miR-132-3p、SIRT1 mRNA表达变化;Western blot检测EMT相关蛋白及SIRT1、NF-κB蛋白表达水平;双荧光素酶验证miR-132-3p、SIRT1靶向关系。结果 研究组miR-132-3p表达较对照组明显增加,而SIRT1 mRNA表达降低(P<0.05);miR-132-3p抑制剂组miR-132-3p、E-cadherin、p-NF-κBp65/NF-κBp65表达较抑制剂阴性组、空白组降低,增殖率、侵袭数、迁移率、vimentin、N-cadherin、SIRT1表达增加(P<0.05);miR-132-3p过表达组miR-132-3p、E-cadherin、p-NF-κBp65/NF-κBp65表达较模拟物阴性组增加,增殖率、侵袭数、迁移率、vimentin、N-cadherin、SIRT1表达降低(P<0.05);miR-132-3p抑制剂+干扰SIRT1组E-cadherin、p-NF-κBp65/NF-κBp65表达较miR-132-3p抑制剂+干扰阴性组增加(P<0.05),增殖率、侵袭数、迁移率、vimentin、N-cadherin、SIRT1表达均降低(P<0.05)。结论 抑制miR-132-3p表达靶向激活SIRT1/NF-κB通路促进滋养层细胞EMT、增殖、侵袭与迁移。

关键词: 上皮-间质转化, SIRT1/NF-κB通路, miR-132-3p, 滋养层细胞

Abstract: Objective To investigate the effect of miR-132-3p on epithelial-mesenchymal transition (EMT) of trophoblast cells through targeted regulation of the SIRT1/NF-κB pathway. Methods Placental tissues from 37 preeclampsia (PE) patients who underwent cesarean section in Zhengzhou Women & Infants Hospital and 37 normal pregnant women who underwent cesarean section were collected as the research group and control group, respectively. RT-qPCR was performed to detect the expression of miR-132-3p and SIRT1 in tissues. During the logarithmic proliferation phase, HTR-8/SVneo cells were grouped into inhibitor negative group, miR-132-3p inhibitor group, mimic negative group, miR-132-3p overexpression group, miR-132-3p inhibitor+interference negative group, and miR-132-3p inhibitor+interference SIRT1 group, with untransfected HTR-8/SVneo cells as the blank group. CCK-8, Transwell assay, scratch assay, and RT-qPCR were used to detect the proliferation, invasion, migration, and changes in miR-132-3p and SIRT1 mRNA expression of HTR-8/SVneo cells. Western blot was used to detect the expression levels of EMT related proteins and SIRT1, NF-κB proteins. Dual luciferase was used to validate the targeting relationship between miR-132-3p and SIRT1. Results The level of miR-132-3p in the research group was significantly higher than that in the control group, while the SIRT1 mRNA was lower (P<0.05). The level of miR-132-3p, E-cadherin, p-NF-κBp65/NF-κBp65 in the miR-132-3p inhibitor group was lower than those in the inhibitor negative group and blank group. The proliferation rate, invasion cell number, migration rate, level of vimentin, N-cadherin, and SIRT1 were all higher (P<0.05). The miR-132-3p, E-cadherin, p-NF-κBp65/NF-κBp65 in the miR-132-3p overexpression group were higher than those in the mimic negative group, the proliferation rate, invasion number, migration rate, vimentin, N-cadherin, and SIRT1 were lower (P<0.05). The level of E-cadherin and p-NF-κBp65/NF-κBp65 in the miR-132-3p inhibitor+interference SIRT1 group was higher than those in the miR-132-3p inhibitor+interference negative group (P<0.05), the proliferation rate, invasion number, migration rate, vimentin, N-cadherin, and SIRT1 expression were lower (P<0.05). MiR-132-3p targeted regulation of SIRT1 expression (P<0.05). Conclusions Inhibition of miR-132-3p promotes the EMT, proliferation, invasion, and migration of trophoblast cells by targeting and activating the SIRT1/NF-κB pathway.

Key words: epithelial-mesenchymal transition, SIRT1/NF-κB pathway, miR-132-3p, trophoblast cells

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