Zinc Finger Protein 90 Knockdown Promotes Cisplatin Sensitivity via Nrf2/HO-1 Pathway in Ovarian Cancer Cell

Simple Summary Our data suggested that cisplatin treatment generates reactive oxygen species (ROS) that modulate apoptotic proteins expression (p-P38, p-ERK, p-Akt, Bcl-2, Bax, active caspase-3). The anti-oxidative signal (Nrf2, HO-1, SOD) was also activated, which could inhibit cell migration (MMP-2, MMP-9, E-cadherin). The intervention of Zfp90 could significantly enhance the apoptosis pathway and inhibit the migrative pathway to regulate the cisplatin sensitivity in ovarian cancer (OC) cells. Our study discussed the role of Zfp90 in ovarian cancer (OC) cell lines' sensitivity to cisplatin. We used two OC cell lines, SK-OV-3 and ES-2, to evaluate their role in cisplatin sensitization. The protein levels of p-Akt, ERK, caspase 3, Bcl-2, Bax, E-cadherin, MMP-2, MMP-9 and other drug resistance-related molecules, including Nrf2/HO-1, were discovered in the SK-OV-3 and ES-2 cells. We also used a human ovarian surface epithelial cell to compare the effect of Zfp90. Our outcomes indicated that cisplatin treatment generates reactive oxygen species (ROS) that modulate apoptotic protein expression. The anti-oxidative signal was also stimulated, which could hinder cell migration. The intervention of Zfp90 could greatly improve the apoptosis pathway and block the migrative pathway to regulate the cisplatin sensitivity in the OC cells. This study implies that the loss of function of Zfp90 might promote cisplatin sensitization in OC cells via regulating the Nrf2/HO-1 pathway to enhance cell apoptosis and inhibit the migrative effect in both SK-OV-3 and ES-2 cells.