Effect of sufentanil on the proliferation, apoptosis, and epithelial-mesenchymal transition of ovarian cancer cells by regulating the SMAD3/SNAIL signaling pathway

To study sufentanil’s effect on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of ovarian cancer cells by modulating the SMAD3/SNAIL signaling pathway. Ovarian cancer A2780 cells were exposed to sufentanil at varying concentrations of 0 ng/mL, 20 ng/mL, 40 ng/mL, 60 ng/mL, 80 ng/mL, and 100 ng/mL. The proliferation of A2780 cells was assessed using the CCK-8 method; A2780 cells were randomly divided into three groups: CON group (normal culture), SUF group (60 ng/mL sufentanil intervention), and SUF + ACA group (60 ng/mL sufentanil and 100 ng/mL activin A intervention). After 48 h of culture, cell migration was evaluated by the scratch assay; Cell invasion was assessed using the Transwell chamber assay; Cell apoptosis was measured via flow cytometry; The growth status of the cells was observed under an optical microscope; The expression of N-cadherin, E-cadherin, SMAD3, TGF-β, and SNAIL proteins was detected by Western blot. When the concentration of sufentanil was ≥ 20 ng/mL, it dose-dependently inhibited the proliferation of ovarian cancer A2780 cells; In comparison to the CON group, the number of A2780 cells in the SUF group was significantly reduced, some cells detached, cell migration and invasion abilities, and the expression levels of N-cadherin, SMAD3, TGF-β, and SNAIL proteins decreased, while the apoptosis rate and E-cadherin protein expression levels increased (P < 0.05); In comparison to the SUF group, the growth status of A2780 cells in the SUF + ACA group was good, cell migration and invasion abilities, and the expression levels of N-cadherin, SMAD3, TGF-β, and SNAIL proteins increased, while the apoptosis rate and E-cadherin protein expression levels decreased (P < 0.05). Sufentanil may inhibit the proliferation and epithelial-mesenchymal transition of ovarian cancer cells and promote cell apoptosis by inhibiting the SMAD3/SNAIL signaling pathway.