Nanotechnology Utilizing Ferroptosis Inducers in Cancer Treatment.

Current cancer treatment options have presented numerous challenges in terms of reaching high efficacy. As a result, an immediate step must be taken to create novel therapies that can achieve more than satisfying outcomes in the fight against tumors. Ferroptosis, an emerging form of regulated cell death (RCD) that is reliant on iron and reactive oxygen species, has garnered significant attention in the field of cancer therapy. Ferroptosis has been reported to be induced by a variety of small molecule compounds known as ferroptosis inducers (FINs), as well as several licensed chemotherapy medicines. These compounds' low solubility, systemic toxicity, and limited capacity to target tumors are some of the significant limitations that have hindered their clinical effectiveness. A novel cancer therapy paradigm has been created by the hypothesis that ferroptosis induced by nanoparticles has superior preclinical properties to that induced by small drugs and can overcome apoptosis resistance. Knowing the different ideas behind the preparation of nanomaterials that target ferroptosis can be very helpful in generating new ideas. Simultaneously, more improvement in nanomaterial design is needed to make them appropriate for therapeutic treatment. This paper first discusses the fundamentals of nanomedicine-based ferroptosis to highlight the potential and characteristics of ferroptosis in the context of cancer treatment. The latest study on nanomedicine applications for ferroptosis-based anticancer therapy is then highlighted.

Ferroptosis Inducers as Promising Radiosensitizer Agents in Cancer Radiotherapy.

Radiotherapy (RT) failure has historically been mostly attributed to radioresistance. Ferroptosis is a type of controlled cell death that depends on iron and is caused by polyunsaturated fatty acid peroxidative damage. Utilizing a ferroptosis inducer may be a successful tactic for preventing tumor growth and radiotherapy-induced cell death. A regulated form of cell death known as ferroptosis is caused by the peroxidation of phospholipids containing polyunsaturated fatty acids in an iron-dependent manner (PUFA-PLs). The ferroptosis pathway has a number of important regulators. By regulating the formation of PUFA-PLs, the important lipid metabolism enzyme ACSL4 promotes ferroptosis, whereas SLC7A11 and (glutathione peroxidase 4) GPX4 prevent ferroptosis. In addition to introducing the ferroptosis inducer chemicals that have recently been demonstrated to have a radiosensitizer effect, this review highlights the function and methods by which ferroptosis contributes to RT-induced cell death and tumor suppression in vitro and in vivo.