Potential mechanism of ferroptosis in pancreatic cancer

Despite the incidence rates of pancreatic cancer being low worldwide, the mortality rates remain high. To date, there is no effective drug treatment for pancreatic cancer. Numerous signalling pathways and cytokines regulate the occurrence and development of pancreatic cancer. Ferroptosis is a non-traditional form of cell death resulting from iron-dependent lipid peroxide accumulation. Studies have demonstrated that ferroptosis is associated with a variety of different types of cancer, such as breast cancer, hepatocellular carcinoma and pancreatic cancer. The present study demonstrated that ferroptosis controls the growth and proliferation of pancreatic cancer, providing a new approach for the treatment of pancreatic cancer. Iron metabolism and reactive oxygen species metabolism are the key pathways involved in ferroptosis in pancreatic cancer. In addition, a number of regulators of ferroptosis, such as glutathione peroxidase 4 and the cystine/glutamate antiporter system Xc-, also play pivotal roles in the regulation of ferroptosis. In the present review, the regulatory mechanisms associated with ferroptosis in pancreatic cancer are summarized, alongside other associated forms of digestive system cancer. The treatment of ferroptosis-based diseases is also addressed.