Abstract
Ferroptosis is a new type of regulatory cell death that differs from autophagy, apoptosis, necrosis, and pyroptosis; it is caused primarily by the accumulation of iron and lipid peroxides in the cell. Studies have shown that many classical signaling pathways and biological processes are involved in the process of ferroptosis. In recent years, investigations have revealed that ferroptosis plays a crucial role in the progression of tumors, especially lung cancer. In particular, inducing ferroptosis in cells can inhibit the growth of tumor cells, thereby reversing tumorigenesis. In this review, we summarize the characteristics of ferroptosis from its underlying basis and role in lung cancer and provide possible applications for it in lung cancer therapies.
Highlights
Lung cancer is among the leading causes of death worldwide and is the primary reason people die in China; it resulted in more than 2.8 million Chinese deaths in 2015, with over 40% of the total number related to lung adenocarcinomas [1]
Transferrin receptor protein 1 (TFR1) is highly expressed in 88% of non-small-cell lung cancer (NSCLC) [6], which suggests that lung cancer cells could increase iron intake by enhancing the effects of the transferrin protein (TF) and TFR
Type I ferroptosis inducers refer to the inhibitors of system xc−, such as erastin, sulfasalazine, and sorafenib, that can reduce the acquisition of cystine by cells, hindering the synthesis of glutathione, a substrate of Glutathione peroxidase 4 (GPX4), and triggering the accumulation of lipid reactive oxygen species and subsequently, ferroptosis
Summary
Lung cancer is among the leading causes of death worldwide and is the primary reason people die in China; it resulted in more than 2.8 million Chinese deaths in 2015, with over 40% of the total number related to lung adenocarcinomas [1]. Ferroptosis is a new type of regulatory cell death that is caused by iron-dependent lipid peroxidation. This new form of regulatory cell death is characterized primarily by reduced cell volume and increased mitochondrial membrane density, without the typical manifestations of apoptosis and necrosis [7]. Cancer cells require significant amounts of iron to survive and grow compared to normal, noncancer cells. This dependence on iron makes cancer cells more susceptible to iron-catalyzed cell death, known as ferroptosis [8]. Targeting ferroptosis could provide a new and promising approach to killing therapy-resistant cancers
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