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