Reactive chlorine species (RCS) are alternatives to reactive oxygen species (ROS) in tumor therapeutics. Unlike ROS, whose generation is limited by hypoxic conditions or insufficient H2O2 levels in the tumor, RCS can be generated through the electrochemical oxidation of abundant Cl- present in body fluids. However, traditional electrochemical therapy modalities have shown suboptimal outcomes. Herein, a flexible anodic electrode is fabricated by growing a carbon nanowire network (C-NWN) onto carbon cloth (CC). Attributing to its excellent hydrophilicity, high specific surface area, and electrochemical surface area, CC@C-NWN demonstrates a superior capability for RCS generation. Additionally, the carbon vacancies in CC@C-NWN not only enhance Cl- adsorption but also reduce the reaction free energy of the chlorine evolution reaction (CER) more significantly compared to that of the oxygen evolution reaction, thereby promoting the CER process. RCS generated from the CC@C-NWN electrochemical system induces severe oxidative stress, disrupting the redox homeostasis in tumor cells and promoting the synergistic anti-tumor effect of apoptosis and ferroptosis. The pliability of CC@C-NWN enables it to conform closely to the tumor, and it has demonstrated remarkable tumor-suppressive efficacy under low-voltage (3 V) condition in in vivo experiments. Therefore, the work holds significant promise for the development of novel tumor treatment strategies.

Gastrointestinal malignancies are a major public health concern worldwide, characterized by high incidence and mortality rates. Despite continuous advancements in existing treatment methods, overall survival rates remain low. Lipid metabolism plays a crucial role in the occurrence, progression, and treatment of gastrointestinal malignancies. Its involvement in the metabolic reprogramming of tumor cells, regulation of the tumor microenvironment, and drug response has become a research hotspot.

This review summarizes current research related to lipid metabolism mechanisms, biomarkers, and therapies in GI cancers, with emphasis on its interaction with the tumor microenvironment.

Our previous studies showed HMGB3 expression may correlate with immunotherapy efficacy in breast cancer patients. Here, we investigated whether HMGB3 overexpression has an impact on anti-PD-1 therapy in triple-negative breast cancer (TNBC) and its molecular mechanisms. Animal models were established to observe the effect of HMGB3 on sensitivity to anti-PD-1 treatment. Correlation of HMGB3 expression and ferroptosis preventive proteins in TNBC patients' tissues with anti-PD-1 therapy efficacy was analyzed. The impact of HMGB3 on IFN-γ (Interferon-gamma) inhibitory effects and signaling was examined in human TNBC cells where HMGB3 expression was knocked down using siRNA. Moreover, TNBC cells stably transfected with lentiviral vectors containing cDNA of HMGB3 were also used to confirm the effect of overexpression of HMGB3 on IFN-γ inhibitory effect and signaling. Effect of HMGB3 on IFN-γ-driven ferroptosis and ferroptosis-associated protein expression were also investigated. Correlation of HMGB3 and IRF1 and GPX4 expression in patient's cancer tissue were also investigated. Our results demonstrated that HMGB3 expression contributes to resistance to anti-PD-1 therapy in vivo. HMGB3 expression correlated with treatment efficacy of immunotherapy and survival in TNBC patients. HMGB3 silence decreased resistance of breast cancer cells to IFN-γ cytotoxic effect, while HMGB3 overexpression increased resistance of these cancer cells. HMGB3 silence increased STAT1 phosphorylation and IRF1 expression upon IFN-γ treatment compared with control. Overexpression of HMGB3 inhibited STAT1 phosphorylation and IFN-γ signaling in TNBC cells. Moreover, HMGB3 also increased STAT3 activation and had an effect of interaction between STAT1 and STAT3. HMGB3 overexpression decreased IFN-γ-driven ferroptosis in TNBC cells. HMGB3 increased ferroptosis-inhibitory proteins (SLC7A11, GPX4, and SLC3A2) expression in TNBC cells. Ferroptosis inhibition recovers resistance to anti-PD-1 therapy in vivo. Immunohistochemistry showed HMGB3 expression correlated with ferroptosis-associated proteins and IRF1 expression in breast cancer tissue. HMGB3 contributes to anti-PD-1 resistance by inhibiting IFN-γ-driven ferroptosis in TNBC which suggested HMGB3 is a potential co-target with anti-PD-1 therapy for TNBC.

Ferroptosis, as a novel modality of cell death, holds significant potential in elucidating the pathogenesis and advancing therapeutic strategies for breast cancer.

This study aims to comprehensively analyze current ferroptosis research and future trends, guiding breast cancer research advancements and innovative treatment strategies.

This research used the R package Bibliometrix (Department of Economic and Statistical Sciences at the University of Naples Federico II), VOSviewer (Centre for Science and Technology Studies at Leiden University), and CiteSpace (Drexel University's College of Information Science and Technology), to conduct a bibliometric analysis of 387 papers on breast cancer and ferroptosis from the Web of Science Core Collection. The analysis covers authors, institutions, journals, countries or regions, publication volumes, citations, and keywords.

The number of publications related to this field has surged annually, with China and the United States collaborating closely and leading in output. Sun Yat-sen University stands out among the institutions, while the journal Frontiers in Oncology and the author Efferth T contribute significantly to the field. Highly cited papers within the domain primarily focus on the induction of ferroptosis, protein regulation, and comparisons with other modes of cell death, providing a foundation for breast cancer treatment. Keyword analysis highlights the maturity of glutathione peroxidase 4-related research, with breast cancer subtypes emerging as motor themes and the tumor microenvironment, immunotherapy, and prognostic models identified as basic themes. Furthermore, the application of nanoparticles serves as an additional complement to the basic themes.

The current research status in the field of ferroptosis and breast cancer primarily focuses on the exploration of relevant theoretical mechanisms, whereas future trends and mechanisms emphasize the investigation of therapeutic strategies, particularly the clinical application of immunotherapy related to the tumor microenvironment. Nanotherapy has demonstrated significant clinical potential in this domain. Future research directions should deepen the exploration in this field and accelerate the clinical translation of research findings to provide new insights and directions for the innovation and development of breast cancer treatment strategies.

Ovarian cancer remains a significant challenge due to the lack of effective treatment and the resistance to conventional therapies. Ferroptosis, a form of regulated cell death characterized by iron-depend and lipid peroxidation, has emerged as a potential therapeutic target in cancer. Ovarian cancer has been reported to exert an "iron addiction" phenotype which makes it is susceptible to ferroptosis inducers. However, we found here that high-adhesion ovarian cancer cells were resistant to ferroptosis. Mechanistically, by PCR array, we identified junctional adhesion molecule 3 (JAM3) as a key mediator of ferroptosis resistance in high-adhesion ovarian cancer cells. Knockdowning and blocking JAM3 sensitized cancer cells to ferroptosis inducers RSL3 and erastin, while JAM3 overexpression conferred resistance to these agents. In addition, JAM3 also promoted ovarian cancer cells resistance to chemotherapeutic agent cisplatin in vitro and in vivo by inhibiting ferroptosis. Furthermore, we demonstrated that JAM3 promoted ferroptosis resistance through NRF2-induced upregulation of FSP1, a critical suppressor of lipid peroxidation. Inhibition of the NRF2/FSP1 pathway eliminated high-adhesion, JAM3 overexpressed ovarian cancer cells resistance to ferroptosis, and decreased cancer cells resistance to cisplatin. Moreover, JAM3 high expression was associated with poor prognosis in patients with ovarian cancer. Altogether, this study provided novel insights into the molecular mechanisms underlying ferroptosis resistance and identify JAM3 as a potential therapeutic target for combating drug resistance in ovarian cancer.

As a pivotal branch of metabolomics, lipidomics studies global changes in lipid metabolism under different physiological and pathological conditions or drug interventions, discovers key lipid markers, and elaborates the associated lipid metabolism network. There are a considerable number of lipids in the host, which act on various functional networks such as metabolism and immune regulation. As an indispensable research method, lipidomics plays a key character in the analysis of lipid composition in organisms, the elaboration of the physiological mechanism of lipids, and the decoding of their character in the occurrence and development of diseases by exploring the character of lipids in the host environmental network. As an essential means of driving lipidomics research, High-throughput and High-resolution mass spectrometry is helpful in exploring disease phenotypic characteristics, diagnosing disease biomarkers, regulating related metabolic pathways, and discovering related active components. In this paper, we discuss the specific role of lipidomics in the analysis of disease diagnosis, prognosis and treatment, which is conducive to the realization of accurate and personalized medicine.

Ferroptosis, a type of programmed cell death, represents a distinct paradigm in cell biology. It is characterized by the iron-dependent accumulation of reactive oxygen species, which induce lipid peroxidation (LPO), and is orchestrated by the interplay between iron, lipid peroxides, and glutathione. In this review, we emphasize the frequently overlooked role of iron in LPO beyond the classical iron-driven Fenton reaction in several crucial processes that regulate cellular iron homeostasis, including iron intake and export as well as ferritinophagy, and the emerging roles of endoplasmic reticulum-resident flavoprotein oxidoreductases, especially P450 oxidoreductases, in modulating LPO. We summarize how various types of fatty acids (FAs), including saturated, monounsaturated, and polyunsaturated FAs, differentially influence ferroptosis when incorporated into phospholipids. Furthermore, we highlight the therapeutic potential of targeting LPO to mitigate ferroptosis and discuss the regulatory mechanisms of endogenous lipophilic radical-trapping antioxidants that confer resistance to ferroptosis, shedding light on therapeutic avenues for ferroptosis-associated diseases.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), which is widely used as an antiozonant in rubber tires, has recently got much attention for its acute aquatic toxicity. However, the developmental toxicity of 6PPD in cerebrovascular network remains unknown. Here, we investigated the effects of 6PPD exposure in cerebral vascular using zebrafish. 6PPD would not affect the body length and shape of zebrafish larvae at the concentrations ranging from 20 μg/L to 1000 μg/L. 6PPD induced developmental defects in the brain in a concentration-dependent manner. The trunk vascular development would not be affected while the cerebrovascular network was disrupted upon 6PPD exposure. 6PPD would trigger excessive Reactive Oxygen Species (ROS) in the brain, indicating abnormal oxidative stress. Mechanistically, brain-specific transcriptome analysis showed that 6PPD could potentially cause the blockage of arachidonic acid (AA) metabolism-related genes and the upregulation of ferroptosis-related genes. Besides, treatment with ferroptosis inhibitor N-Acetyl-L-cysteine (NAC) attenuated oxidative damage and improved the construction of cerebrovascular network upon 6PPD exposure. Moreover, using a human vascular endothelial cell line, we further confirmed that 6PPD could trigger abnormal oxidative stress and defective expansion capacity, implying the conserved toxicity cross species. These findings are useful for the elucidation of toxicity underlying 6PPD in cerebrovascular systems of both zebrafish and humans.

Ferroptosis is an iron-dependent lipid peroxidation-mediated cell death. It is distinct from other types of cellular death and is recognized as a potential target for cancer therapy. This review discusses the mechanisms of ferroptosis, including its induction and inhibition pathways, its role in lipid metabolism, and its connection to various signaling pathways. We also explored the relationship between microRNAs and ferroptosis, highlighting the potential role of miRNAs targeting genes involved in ferroptosis. Role of miRNAs in metabolic reprogramming during carcinogenesis is well documented. We have discussed the role of miRNAs regulating expression of genes involved in iron metabolism, lipid metabolism, and redox metabolism which are associated with regulation of ferroptosis. In conclusion, we addressed various opportunities and challenges identified in ferroptosis research and its clinical implementation stressing the necessity of customized treatment plans based on each patient's unique vulnerability to the disease. Our article provides a complete overview of microRNAs and ferroptosis, with possible implications for cancer therapy.

Ovarian cancer is a malignant tumor originating from the ovary, characterized by its high mortality rate and propensity for recurrence. In some patients, especially those with recurrent cancer, conventional treatments such as surgical resection or standard chemotherapy yield suboptimal results. Consequently, there is an urgent need for novel anti-cancer therapeutic strategies. Ferroptosis is a distinct form of cell death separate from apoptosis. Ferroptosis inducers have demonstrated promising potential in the treatment of ovarian cancer, with evidence indicating their ability to enhance ovarian cancer cell sensitivity to cisplatin. However, resistance of cancer cells to ferroptosis still remains an inevitable challenge. Here, we analyzed genome-scale CRISPR-Cas9 loss-of function screens and identified PAX8 as a ferroptosis resistance protein in ovarian cancer. We identified PAX8 as a susceptibility gene in GPX4-dependent ovarian cancer. Depletion of PAX8 rendered GPX4-dependent ovarian cancer cells significantly more sensitive to GPX4 inhibitors. Additionally, we found that PAX8 inhibited ferroptosis in ovarian cancer cells. Combined treatment with a PAX8 inhibitor and RSL3 suppressed ovarian cancer cell growth, induced ferroptosis, and was validated in a xenograft mouse model. Further exploration of the molecular mechanisms underlying PAX8 inhibition of ferroptosis mutations revealed upregulation of glutamate-cysteine ligase catalytic subunit (GCLC) expression. GCLC mediated the ferroptosis resistance induced by PAX8 in ovarian cancer. In conclusion, our study underscores the pivotal role of PAX8 as a therapeutic target in GPX4-dependent ovarian cancer. The combination of PAX8 inhibitors such as losartan and captopril with ferroptosis inducers represents a promising new approach for ovarian cancer therapy.

This editorial discusses a recently published paper in the World Journal of Gastroenterology. Our research focuses on p53's regulatory mechanism for controlling ferroptosis, as well as the intricate connection between ferroptosis and liver diseases. Ferroptosis is a specific form of programmed cell death that is de-pendent on iron and displays unique features in terms of morphology, biology, and genetics, distinguishing it from other forms of cell death. Ferroptosis can affect the liver, which is a crucial organ responsible for iron storage and meta-bolism. Mounting evidence indicates a robust correlation between ferroptosis and the advancement of liver disorders. P53 has a dual effect on ferroptosis through various distinct signaling pathways. However, additional investigations are required to clarify the regulatory function of p53 metabolic targets in this complex association with ferroptosis. In the future, researchers should clarify the mechanisms by which ferroptosis and other forms of programmed cell death contribute to the progression of liver diseases. Identifying and controlling important regulatory factors associated with ferroptosis present a promising therapeutic strategy for liver disorders.

Breast cancer is a common invasive tumor in women, and the most common subtype of breast cancer is luminal A. Hormonal therapies are the primary treatment for luminal A, but treatment options are limited. Vulpinic acid (VA), a lichen compound, inhibited cancer cells. Here, we aimed to reveal the functional role and mechanism of VA in luminal A breast cancer. Experiments associated with the ferroptosis mechanism were performed to reveal the role of vulpinic acid on luminal A-breast cancer and the underlying mechanisms. The results showed that VA induced the ferroptosis pathway by decreasing glutathione (GSH) levels while increasing lipid reactive oxygen species (ROS), lipid peroxidation (MDA), and intracellular Fe2+ levels in MCF-7 cells. After treatment of MCF-7 cells with VA, the ferroptosis-related gene expression profile was significantly altered. Western blot analysis showed that GPX4 protein levels were down-regulated and LPCAT3 protein levels were up-regulated after VA treatment. Our study suggests that apoptosis and ferroptosis act together in VA-mediated tumor suppression in MCF-7 breast cancer cells. These findings suggest that VA, an anti-neoplastic agent, could potentially treat luminal A targeted breast cancer via the ferroptosis pathway.

Combination therapy has emerged as a promising approach for treating tumors, although there is room for improvement. This study introduced a novel strategy that combined the enhancement of apoptosis, ferroptosis, and DNA damage to improve therapeutic outcomes for prostate cancer. Specifically, we have developed a supramolecular oxidative stress nanoamplifier, which was comprised of β-cyclodextrin, paclitaxel, and ferrocene-poly(ethylene glycol). Paclitaxel within the system disrupted microtubule dynamics, inducing G2/M phase arrest and apoptosis. Concurrently, ferrocene utilized hydrogen peroxide to generate toxic hydroxyl radicals in cells through the Fenton reaction, triggering a cascade of reactive oxygen species expansion, reduction of glutathione levels, lipid peroxidation, and ferroptosis. The increased number of hydroxyl radicals and the inhibitory effect of THZ531 on DNA repair mechanisms exacerbated DNA damage within tumor cells. As expected, the supramolecular nanoparticles demonstrated excellent drug delivery ability to tumor cells or tissues, exhibited favorable biological safety in vivo, and enhanced the killing effect on prostate cancer.

Chondrocyte degeneration and senescence are characteristics of osteoarthritis (OA) and other joint degenerative diseases, and ferroptosis has been observed to regulate the development of OA. However, the role of the N6-methyladenosine (m6A) modification in OA ferroptosis remains unclear.

This study performed series of assays to investigate the function of the m6A reader IGF2BP1 in OA ferroptosis, including m6A quantitative analysis, Iron (Fe2+) release analysis, Malondialdehyde (MDA) measurement, lipid peroxidation (ROS) detection and Glutathione (GSH) measurement. The molecular interaction and mechanism analysis was performed by Luciferase reporter assay, mRNA stability analysis and RNA immunoprecipitation (RIP) assay.

These results indicate that IGF2BP1 is upregulated in IL-1β-induced chondrocytes. Functionally, IGF2BP1 silencing represses ferroptosis, including iron (Fe2+) accumulation, malondialdehyde, and reactive oxygen species (ROS). Mechanistically, among the potential downstream targets, matrix metalloproteinase-3 (MMP3) was observed to harbor a significant m6A modified site in the 3'-UTR. IGF2BP1 combines with MMP3 through the binding of m6A sites, thereby enhancing MMP3 mRNA stability.

In conclusion, our findings revealed the functions and mechanisms of m6A regulator IGF2BP1 in OA chondrocyte's ferroptosis, providing a novel target for OA treatment.

Ferroptosis is a distinct mode of cell death, distinguishing itself from typical apoptosis by its reliance on the accumulation of iron ions and lipid peroxides. Cells manifest an imbalance between oxidative stress and antioxidant equilibrium during certain pathological contexts, such as tumours, resulting in oxidative stress. Notably, recent investigations propose that heightened intracellular reactive oxygen species (ROS) due to oxidative stress can heighten cellular susceptibility to ferroptosis inducers or expedite the onset of ferroptosis. Consequently, comprehending role of ROS in the initiation of ferroptosis has significance in elucidating disorders related to oxidative stress. Moreover, an exhaustive exploration into the mechanism and control of ferroptosis might offer novel targets for addressing specific tumour types. Within this context, our review delves into recent fundamental pathways and the molecular foundation of ferroptosis. Four classical ferroptotic molecular pathways are well characterized, namely, glutathione peroxidase 4-centred molecular pathway, nuclear factor erythroid 2-related factor 2 molecular pathway, mitochondrial molecular pathway, and mTOR-dependent autophagy pathway. Furthermore, we seek to elucidate the regulatory contributions enacted by ROS. Additionally, we provide an overview of targeted medications targeting four molecular pathways implicated in ferroptosis and their potential clinical applications. Here, we review the role of ROS and oxidative stress in ferroptosis, and we discuss opportunities to use ferroptosis as a new strategy for cancer therapy and point out the current challenges persisting within the domain of ROS-regulated anticancer drug research and development.

Ferroptosis, a novel form of regulated cell death characterized by dependence on iron and lipid peroxidation, has been implicated in a wide range of clinical conditions including neurological diseases, cardiovascular disorders, acute kidney failure, and various types of cancer. Therefore, it is critical to suppress cancer progression and proliferation. Ferroptosis can be triggered in cancer cells and some normal cells by synthetic substances, such as erastin, Ras-selective lethal small molecule-3, or clinical pharmaceuticals. Natural bioactive compounds are traditional drug discovery tools, and some have been therapeutically used as dietary additives or pharmaceutical agents against various malignancies. The fact that natural products have multiple targets and minimal side effects has led to notable advances in anticancer research. Research has indicated that ferroptosis can also be induced by natural compounds during cancer treatment. In this review, we focused on the most recent developments in emerging molecular processes and the significance of ferroptosis in cancer. To provide new perspectives on the future development of ferroptosis-related anticancer medications, we also provide a summary of the implications of natural phytochemicals in triggering ferroptosis through ROS production and ferritinophagy induction in a variety of malignancies.

Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death and has been implicated in the occurrence and development of various diseases, including heart disease, nervous system diseases and cancer. Ferroptosis induction recently emerged as an attractive strategy for cancer therapy. Ferroptosis has become a potential target for intervention in these diseases or injuries in relevant preclinical models. This review summarizes recent progress on the mechanisms of ferroptosis resistance in cancer, highlights redox status and metabolism's role in it. Combination therapy for ferroptosis has great potential in cancer treatment, especially malignant tumors that are resistant to conventional therapies. This review will lead us to have a comprehensive understanding of the future exploration of ferroptosis and cancer therapy. A deeper understanding of the relationship between ferroptosis resistance and metabolism reprogramming may provide new strategies for tumor treatment and drug development based on ferroptosis.

Ferroptosis is an iron-dependent programmed cell death mode that is distinct from other cell death modes, and radiation is able to stimulate cellular oxidative stress and induce the production of large amounts of reactive oxygen radicals, which in turn leads to the accumulation of lipid peroxide and the onset of ferroptosis. In this review, from the perspective of the role of ferroptosis in generating a radiation response following cellular irradiation, the relationship between ferroptosis induced by ionizing radiation stress and the response to ionizing radiation is reviewed, including the roles of MAPK and Nrf2 signaling pathways in ferroptosis, resulting from the oxidative stress response to ionizing radiation, the metabolic regulatory role of the p53 gene in ferroptosis, and regulatory modes of action of iron metabolism and iron metabolism-related regulatory proteins in promoting and inhibiting ferroptosis. It provides some ideas for the follow-up research to explore the specific mechanism and regulatory network of ferroptosis in response to ionizing radiation.

Human dihydroorotate dehydrogenase (hDHODH) is a key enzyme that catalyzes the de novo synthesis of pyrimidine. In recent years, various studies have shown that inhibiting this enzyme can treat autoimmune diseases such as rheumatoid arthritis (RA) and cancer. This study designed and synthesized a series of novel thiazolidone hDHODH inhibitors. Through biological activity evaluation, Compound 14 was found to have high inhibitory activity, with an IC50 value reaching nanomolar level. Preliminary structure-activity relationship studies found that the carboxyl group in R1 and the naphthalene in R2 are key factors in improving activity. Through molecular docking, the binding mode between inhibitors and proteins was elucidated. This study provides an important reference for further optimizing hDHODH inhibitors.

Triple-negative breast cancer (TNBC), the most aggressive form of breast cancer, presents severe threats to women's health. Therefore, it is critical to find novel treatment approaches. Ferroptosis, a newly identified form of programmed cell death, is marked by the buildup of lipid reactive oxygen species (ROS) and high iron concentrations. According to previous studies, ferroptosis sensitivity can be controlled by a number of metabolic events in cells, such as amino acid metabolism, iron metabolism, and lipid metabolism. Given that TNBC tumors are rich in iron and lipids, inducing ferroptosis in these tumors is a potential approach for TNBC treatment. Notably, the metabolic adaptability of cancer cells allows them to coordinate an attack on one or more metabolic pathways to initiate ferroptosis, offering a novel perspective to improve the high drug resistance and clinical therapy of TNBC. However, a clear picture of ferroptosis in TNBC still needs to be completely revealed. In this review, we provide an overview of recent advancements regarding the connection between ferroptosis and amino acid, iron, and lipid metabolism in TNBC. We also discuss the probable significance of ferroptosis as an innovative target for chemotherapy, radiotherapy, immunotherapy, nanotherapy and natural product therapy in TNBC, highlighting its therapeutic potential and application prospects.

Ferroptosis, characterized by glutamate overload, glutathione depletion, and cysteine/cystine deprivation during iron- and oxidative-damage-dependent cell death, is a particular mode of regulated cell death. It is expected to effectively treat cancer through its tumor-suppressor function, as mitochondria are the intracellular energy factory and a binding site of reactive oxygen species production, closely related to ferroptosis. This review summarizes relevant research on the mechanisms of ferroptosis, highlights mitochondria's role in it, and collects and classifies the inducers of ferroptosis. A deeper understanding of the relationship between ferroptosis and mitochondrial function may provide new strategies for tumor treatment and drug development based on ferroptosis.

Radiotherapy is applied in about 70% patients with tumors, yet radioresistance of tumor cells remains a challenge that limits the efficacy of radiotherapy. Ferroptosis, an iron-dependent lipid peroxidation regulated cell death, is involved in the development of a variety of tumors. Interestingly, there is evidence that ferroptosis inducers in tumor treatment can significantly improve radiotherapy sensitivity. In addition, related studies show that Glutathione S-transferase P1 (GSTP1) is closely related to the development of ferroptosis. The potential mechanism of targeting GSTP1 to inhibit tumor cells from evading ferroptosis leading to radioresistance has been proposed in this review, which implies that GSTP1 may play a key role in radiosensitization of lung cancer via ferroptosis pathway.