Pharmacological Targeting of Ferroptosis in Cancer Treatment

Abstract

A non-apoptotic iron-dependent form of Regulated Cell Death (RCD) known as ferroptosis is brought on by an excess of harmful lipid peroxides and iron overload. Inhibiting the antioxidant defense system results in overwhelming of GSH dependent pathway and building up iron-dependent Reactive Oxygen Species (ROS) that react with polyunsaturated fatty acids in large quantities can both cause ferroptosis. Recent research has shown that ferroptosis holds a great deal of promise for preventing tumor cell resistance and limiting growth and spread. Emerging evidence also suggests that ferroptosis plays a dual role in human cancer. However, the precise underlying molecular mechanisms and their different role in tumorigenesis are unclear. Therefore, in this review we summarize and briefly present the key pathways of ferroptosis, its dual role as an oncogenic and as a tumor suppressor event in human cancers, paying special attention to the regulation of ferroptosis along with a variety of current medications and naturally occurring substances that may one day be used to target ferroptosis in tumor cells. Thus, addressing this sort of cell death could be seen as a potentially expanding technique in cancer treatment. Consequently, this will offer crucial viewpoints for next research on ferroptosis-based cancer treatment.
 Keywords: Ferroptosis, antioxidant defense system, Cancer