Fig. 7

FA-PBM NPs mechanism to induce apoptosis and inhibit drug resistance in OvCa. This figure summarizes the mechanisms of combination FA-PBM NPs to induce apoptosis and inhibit drug resistance in OvCa cells. Following treatment with FA-PBM NPs, the intrinsic apoptosis pathway is initiated, triggering a cascade of events leading to the synthesis of Bcl-2 family proteins, including pro-apoptotic and anti-apoptotic proteins. The anti-apoptotic proteins, BCL-2, BCL-XL, and MCL1, are downregulated, and the pro-apoptotic proteins, BAX, BAK, and BID, are upregulated, ultimately inducing apoptosis in OvCa cells. Additionally, cytosolic Fis and PTX inhibit the drug efflux pump, ABCG2, reversing multi-drug resistance. Lastly, the anticancer drug could induce the Fas/FasL pathway to activate caspase 3 by proteolytic cleavage or stimulate BID, leading to apoptosis of OvCa cells. This evidence provides insight into how to treat platinum-resistant cancer cells that usually evade apoptosis