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Journal articles on the topic 'Erastin'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Li, Huifang, Ni Deng, Tess Puopolo, et al. "Cannflavins A and B with Anti-Ferroptosis, Anti-Glycation, and Antioxidant Activities Protect Human Keratinocytes in a Cell Death Model with Erastin and Reactive Carbonyl Species." Nutrients 15, no. 21 (2023): 4565. http://dx.doi.org/10.3390/nu15214565.

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Precursors of advanced glycation endproducts, namely, reactive carbonyl species (RCSs), are aging biomarkers that contribute to cell death. However, the impact of RCSs on ferroptosis—an iron-dependent form of cell death—in skin cells remains unknown. Herein, we constructed a cellular model (with human keratinocyte; HaCaT cells) to evaluate the cytotoxicity of the combinations of RCSs (including glyoxal; GO and methyglyoxal; MGO) and erastin (a ferroptosis inducer) using bioassays (measuring cellular lipid peroxidation and iron content) and proteomics with sequential window acquisition of all t

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2

Liu, Nan, Xiaoli Lin, and Chengying Huang. "Activation of the reverse transsulfuration pathway through NRF2/CBS confers erastin-induced ferroptosis resistance." British Journal of Cancer 122, no. 2 (2019): 279–92. http://dx.doi.org/10.1038/s41416-019-0660-x.

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Abstract Background Ferroptosis is an iron-dependent, lipid peroxide-mediated cell death that may be exploited to selective elimination of damaged and malignant cells. Recent studies have identified that small-molecule erastin specifically inhibits transmembrane cystine–glutamate antiporter system xc−, prevents extracellular cystine import and ultimately causes ferroptosis in certain cancer cells. In this study, we aimed to investigate the molecular mechanism underlying erastin-induced ferroptosis resistance in ovarian cancer cells. Methods We treated ovarian cancer cells with erastin and exam

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Naser, Rua Abbas, Inam Sameh Arif, and Basma Talib Al-Sudani. "Erastin Induces Ferroptosis and Apoptosis in MDA-MB-231 Breast Cancer Cell Line." Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ) 8, no. 2 (2025): 168–72. https://doi.org/10.54133/ajms.v8i2.1950.

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Background: Breast cancer (BC) is one of the most malignant types of cancer in women. Triple-negative breast cancer (TNBC) is a subtype of breast cancer with poor prognosis and high recurrence and invasive metastasis rates. Ferroptosis is a non-apoptotic form of cell death characterized by iron-dependent accumulation of reactive oxygen species (ROS). Although ferroptosis induced by erastin has been widely studied, the ability of erastin to induce apoptosis has not been extensively investigated. Objective: To evaluate the effect of erastin on the viability of MDA-MB-231 breast cancer cells and

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4

Oh, Byung Moo, Seon-Jin Lee, Gyoung Lim Park та ін. "Erastin Inhibits Septic Shock and Inflammatory Gene Expression via Suppression of the NF-κB Pathway". Journal of Clinical Medicine 8, № 12 (2019): 2210. http://dx.doi.org/10.3390/jcm8122210.

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Sepsis is a life-threatening condition that is caused by an abnormal immune response to infection and can lead to tissue damage, organ failure, and death. Erastin is a small molecule capable of initiating ferroptotic cell death in cancer cells. However, the function of erastin in the inflammatory response during sepsis remains unknown. Here, we showed that erastin ameliorates septic shock induced by cecal ligation and puncture or lipopolysaccharides (LPS) in mice, which was associated with a reduced production of inflammatory mediators such as nitric oxide, tumor necrosis factor (TNF)-α, and i

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Gao, Wenjin, Chen Mo, Wei Feng, Xinmin Pan, and Haojie Qin. "Research on the Effects of Neuroglobin on Ferroptosis in the Nerve Cells." Chinese medicine and natural products 03, no. 03 (2023): e133-e142. http://dx.doi.org/10.1055/s-0043-1773796.

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Abstract Objectives The objective of this article was to explore the effects of neuroglobin (NGB) on ferroptosis in the nerve cells. Methods The NGB knockdown model of HT22 cells was constructed, and the ferroptosis-related indexes of cell proliferation activity, contents of iron ion, malondialdehyde (MDA), superoxide and reactive oxygen, and the changes of nuclear factor E2-related factor 2 (Nrf2) expression were examined in the normal group, erastin group, NGB siRNA group, and NGB siRNA + Erastin group, respectively. Results Compared with the normal group, cell proliferation activity and Nrf

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Hou, Wanyun, Puze Long, Xilin Liu, et al. "CISD2 protects against Erastin induced hepatocellular carcinoma ferroptosis by upregulating FSP1." Oncologie 25, no. 3 (2023): 269–79. http://dx.doi.org/10.1515/oncologie-2023-0074.

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Abstract Objectives CDGSH iron sulfur domain 2 (CISD2) is essential to maintain iron (Fe) and reactive oxygen species (ROS) homeostasis, and ferroptosis suppressor protein 1 (FSP1) can protect cells from ferroptosis by inhibiting lipid peroxidation. Here, we investigate the role and potential mechanism of CISD2 and FSP1 in ferroptosis of hepatocellular carcinoma (HCC). Methods Human HCC cells were exposed to ferroptosis inducer Erastin, and the expression changes of CISD2 and FSP1 during ferroptosis were detected. Subsequently, we investigated the effect of overexpression of CISD2 on ferroptos

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7

Liu, Weilin, Hongqi Chen, Zhi Zhu, et al. "Ferroptosis Inducer Improves the Efficacy of Oncolytic Virus-Mediated Cancer Immunotherapy." Biomedicines 10, no. 6 (2022): 1425. http://dx.doi.org/10.3390/biomedicines10061425.

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Ferroptosis is a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides. In this study, we explore the combination of a ferroptosis activator with an oncolytic vaccinia virus in tumor models. Erastin induced cell death in hepatoma, colon, and ovarian cancer cells, but not in melanoma cancer cells. Erastin, not the oncolytic vaccinia virus (OVV), induced the expression of key marker genes for ferroptosis in cancer cells. In hepatocellular carcinoma and colon cancer models, either erastin or OVV inhibited tumor growth, but a combination of the tw

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8

Perera, Lalith, Shalyn M. Brown, Brian B. Silver, Erik J. Tokar, and Birandra K. Sinha. "Ferroptosis Inducers Erastin and RSL3 Enhance Adriamycin and Topotecan Sensitivity in ABCB1/ABCG2-Expressing Tumor Cells." International Journal of Molecular Sciences 26, no. 2 (2025): 635. https://doi.org/10.3390/ijms26020635.

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Acquired resistance to chemotherapeutic drugs is the primary cause of treatment failure in the clinic. While multiple factors contribute to this resistance, increased expression of ABC transporters—such as P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and multidrug resistance proteins—play significant roles in the development of resistance to various chemotherapeutics. We found that Erastin, a ferroptosis inducer, was significantly cytotoxic to NCI/ADR-RES, a P-gp-expressing human ovarian cancer cell line. Here, we examined the effects of both Erastin and RSL3 (Ras-Selected L

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9

Liu, Yawen, Pu Huang, Zheng Li, et al. "Vitamin C Sensitizes Pancreatic Cancer Cells to Erastin-Induced Ferroptosis by Activating the AMPK/Nrf2/HMOX1 Pathway." Oxidative Medicine and Cellular Longevity 2022 (July 19, 2022): 1–15. http://dx.doi.org/10.1155/2022/5361241.

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Ferroptosis is a type of regulated cell death that displays a promising therapeutic pathway for drug-resistant tumor cells. However, some pancreatic cancer (PC) cells are less sensitive to erastin-induced ferroptosis, and normal pancreatic cells are susceptible to this newly discovered cell death. Therefore, there is an urgent need to find drugs to enhance the sensitivity of these PC cells to erastin while limiting side effects. Here, we found that the oxidized form of vitamin C-dehydroascorbic acid (DHA) can be transported into PC cells expressing high levels of GLUT1, resulting in ferroptosi

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Al-Hamdy, Rua Abbas Naser, Inam Sameh Arif, and Basma Talib Al-Sudani. "SHIP2 Silencing Enhances Erastin Cytotoxicity in MDA-MB-231 Breast Cancer Cell Line." Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ) 8, no. 2 (2025): 182–87. https://doi.org/10.54133/ajms.v8i2.1916.

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Background: Breast cancer (BC) is a serious health risk to women worldwide. Triple-negative breast cancer (TNBC) is a highly heterogeneous type of breast cancer that is highly malignant, recurrent, and invasive. Despite cancer treatment having developed rapidly in the past decades, TNBC is still having challenges. Erastin is an inducer of ferroptosis and inhibits tumor cell growth, thus making it a promising strategy for cancer therapy. The SH2-containing 5´ inositol phosphatase 2 (SHIP2) is overexpressed in BC, where it is associated with poor prognosis. Objective: To address the effect of er

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Kose, Tugba, Paul A. Sharp, and Gladys O. Latunde-Dada. "Antioxidative Effects of Curcumin on Erastin-Induced Ferroptosis Through GPX4 Signalling." Gastrointestinal Disorders 7, no. 1 (2025): 4. https://doi.org/10.3390/gidisord7010004.

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Background/Objectives: Pancreatic cancer is a common gastrointestinal cancer with high risk of mortality. Currently, the therapeutic strategies for pancreatic cancers are surgery, chemotherapy, and radiotherapy, none of which are effective treatments. Ferroptosis is a new form of cell death that is iron (Fe)-dependent and characterized by lipid peroxidation, which is a new approach for treatment of pancreatic cancer. Therefore, this study was dedicated to investigating the effect of erastin and Ras-selective lethal small molecule 3 (RLS3) as ferroptosis inducers as well as focusing on the anti

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Kose, Tugba, Paul A. Sharp, and Gladys O. Latunde-Dada. "Upregulation of Nrf2 Signalling and the Inhibition of Erastin-Induced Ferroptosis by Ferulic Acid in MIN6 Cells." International Journal of Molecular Sciences 23, no. 24 (2022): 15886. http://dx.doi.org/10.3390/ijms232415886.

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Ferroptosis is a regulated cell death process characterised by the iron-dependent accumulation of oxidised polyunsaturated fatty acid-containing phospholipids. Its initiation is complicated and involves reactive oxygen species (ROS) and a loss of the activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4). These play critical roles in the development of ferroptotic cell damage by lipid peroxidation. Antioxidant therapy is a promising therapeutic strategy to prevent or even reverse the progression of ferroptosis. This study was designed to demonstrate the protective effect of feruli

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13

Liu, Ching-Hsuan, and Yuan-Yu Lin. "PSI-16 Intestinal Porcine Enterocyte Cell (Ipec-J2) as an In-Vitro Model for Investigating the Mechanisms of Ferroptosis." Journal of Animal Science 101, Supplement_3 (2023): 372–73. http://dx.doi.org/10.1093/jas/skad281.442.

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Abstract Ferroptosis is a newly identified form of regulated cell death that has been implicated in various intestinal diseases. However, there is limited research on ferroptosis in porcine models. The aim of this study was to establish an in vitro model of ferroptosis in the IPEC-J2 cell line. Ferroptosis is a form of regulated cell death that was first identified in 2012 and is characterized by unique morphological and physiological features that distinguish it from other types of cell death. This process is triggered by a complex interplay of multiple factors, including excess ferrous iron

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Borisova, L. M., V. N. Osipov, I. S. Golubeva, M. P. Kiseleva, D. A. Hochenkov, and A. A. Vartanyan. "3-Hydroxyquinazoline derivatives, analogues of erastin, induced ferroptosis in breast cancer cells." Advances in Molecular Oncology 9, no. 1 (2022): 48–56. http://dx.doi.org/10.17650/2313-805x-2022-9-1-48-56.

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Introduction. Early malignant tumor detection programs have significantly increased the survival rate of breast cancer patients but the results of drug therapy for this pathology are not always highly effective. Recently discovered iron-dependent cell death, ferroptosis, makes it a promising therapeutic target to reduce the recurrence rates.Objective – to study the induction of ferroptosis in breast cancer cells MCF-7 by quinazoline derivatives synthesized at the Research Institute of Experimental Diagnostics and Therapy of Tumors of the N.N. Blokhin National Medical Research Center of Oncolog

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15

Guo, Shihui, Aiying Zhong, Dongxu Zhang, et al. "ATP2B3 Inhibition Alleviates Erastin–Induced Ferroptosis in HT-22 Cells through the P62–KEAP1–NRF2–HO-1 Pathway." International Journal of Molecular Sciences 24, no. 11 (2023): 9199. http://dx.doi.org/10.3390/ijms24119199.

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Ferroptosis participates in the occurrence and development of neurological disorders. Modulating ferroptosis may have therapeutic potential in nervous system diseases. Therefore, TMTbased proteomic analysis in HT-22 cells was performed to identify erastin–induced differentially expressed proteins. The calcium-transporting ATP2B3 (ATP2B3) was screened as a target protein. ATP2B3 knockdown markedly alleviated the erastin–induced decrease in cell viability and elevated ROS (p < 0.01) and reversed the up-regulation of oxidative stress-related proteins polyubiquitin-binding protein p62 (P62), nu

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Su, Li, Yi Huang, Lei Zheng, Zhifa Zhu, Yue Wu, and Ping Li. "Isocitrate dehydrogenase 1 mutation in cholangiocarcinoma impairs tumor progression by sensitizing cells to ferroptosis." Open Medicine 17, no. 1 (2022): 863–70. http://dx.doi.org/10.1515/med-2022-0477.

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Abstract The present study intends to clarify the hypothesis that isocitrate dehydrogenase 1 (IDH1) mutation in cholangiocarcinoma impairs tumor progression by sensitizing cells to ferroptosis through the in vitro and in vivo experiments. Cholangiocarcinoma RBE cell line was transfected with IDH1 R132C mutation plasmids and treated with erastin to induce ferroptosis, which were then microscopically photographed. Cell viability rate was calculated by trypan blue staining. The lipid ROS level was determined by using flow cytometer. The BALB/c nude mice were injected subcutaneously with IDH1 knoc

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17

Valanezhad, Alireza, Tetsurou Odatsu, Shigeaki Abe, and Ikuya Watanabe. "Bone Formation Ability and Cell Viability Enhancement of MC3T3-E1 Cells by Ferrostatin-1 a Ferroptosis Inhibitor of Cancer Cells." International Journal of Molecular Sciences 22, no. 22 (2021): 12259. http://dx.doi.org/10.3390/ijms222212259.

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Recently, ferroptosis has gained scientists’ attention as an iron-related regulated necrosis. However, not many reports have investigated the effect of ferroptosis on bone. Therefore, with the present study, we assessed the effect of ferroptosis inhibition using ferrostatin-1 on the MC3T3-E1 pre-osteoblast cell. Cell images, cell viability, alkaline phosphatase activity test, alizarin red staining, and RUNX2 gene expression using real-time PCR were applied to investigate the effects of ferrostatin and erastin on MC3T3-E1 osteoblast cells. Erastin was used as a well-known ferroptosis inducer re

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Savic, Dragana, Teresa Bernadette Steinbichler, Julia Ingruber, et al. "Erk1/2-Dependent HNSCC Cell Susceptibility to Erastin-Induced Ferroptosis." Cells 12, no. 2 (2023): 336. http://dx.doi.org/10.3390/cells12020336.

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Unfavorable clinical outcomes mean that cancer researchers must attempt to develop novel therapeutic strategies to overcome therapeutic resistance in patients with HNSCC. Recently, ferroptosis was shown to be a promising pathway possessing druggable targets, such as xCT (SLC7A11). Unfortunately, little is known about the molecular mechanisms underlying the susceptibility of HNSCC cells to ferroptosis. The goal of this study was to determine whether HNSCC cells with activated Erk1/2 are vulnerable to ferroptosis induction. Our results have shown that xCT (SLC7A11) was overexpressed in malignant

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Kose, Tugba, Mayra Vera-Aviles, Paul A. Sharp, and Gladys O. Latunde-Dada. "Curcumin and (−)- Epigallocatechin-3-Gallate Protect Murine MIN6 Pancreatic Beta-Cells Against Iron Toxicity and Erastin-Induced Ferroptosis." Pharmaceuticals 12, no. 1 (2019): 26. http://dx.doi.org/10.3390/ph12010026.

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Ferroptosis is a form of programmed cell death that is characterized by lipid peroxidation and is inducible by iron and the accumulation of reactive oxygen species (ROS). It is triggered by erastin but inhibited by antioxidants such as -tocopherol, -carotene, polyphenols, and iron chelators such as deferoxamine (DFO), nitrilotriacetic acid (NTA), and ethylenediaminetetraacetic acid (EDTA). This study investigated the protective effects of two polyphenols, curcumin and (−)- epigallocatechin-3-gallate (EGCG), against iron loading and erastin-mediated ferroptosis in MIN6 cells. Cells were treated

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Brown, Shalyn M., Birandra K. Sinha, and Ronald E. Cannon. "A Role for iNOS in Erastin Mediated Reduction of P-Glycoprotein Transport Activity." Cancers 16, no. 9 (2024): 1733. http://dx.doi.org/10.3390/cancers16091733.

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The blood–brain barrier is composed of both a physical barrier and an enzymatic barrier. Tight junction (TJ) proteins expressed between endothelial cells of brain capillaries provide the physical barrier to paracellular movement of ions and molecules to the brain, while luminal-facing efflux transporters enzymatically restrict the entry of blood-borne molecules from entering the brain. The expression and activity of ATP Binding Cassette transporters or “ABC” transporters in endothelial cells of the BBB and in human tumor cells are dynamically regulated by numerous signaling pathways. P-glycopr

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Adedoyin, Oreoluwa, Ravindra Boddu, Amie Traylor, et al. "Heme oxygenase-1 mitigates ferroptosis in renal proximal tubule cells." American Journal of Physiology-Renal Physiology 314, no. 5 (2018): F702—F714. http://dx.doi.org/10.1152/ajprenal.00044.2017.

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Ferroptosis is an iron-dependent form of regulated nonapoptotic cell death, which contributes to damage in models of acute kidney injury (AKI). Heme oxygenase-1 (HO-1) is a cytoprotective enzyme induced in response to cellular stress, and is protective against AKI because of its antiapoptotic and anti-inflammatory properties. However, the role of HO-1 in regulating ferroptosis is unclear. The purpose of this study was to elucidate the role of HO-1 in regulating ferroptotic cell death in renal proximal tubule cells (PTCs). Immortalized PTCs obtained from HO-1+/+ and HO-1−/− mice were treated wi

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Giarrizzo, Michael, Joseph F. LaComb, Hetvi R. Patel, et al. "Abstract 659: TR-107 and erastin produce synergistic inhibition of colorectal cancer cell viability in vitro." Cancer Research 84, no. 6_Supplement (2024): 659. http://dx.doi.org/10.1158/1538-7445.am2024-659.

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Abstract Introduction: Ferroptosis is an emerging potential target for the treatment of colorectal cancer (CRC) and has been shown to sensitize cancer cells to combinatory chemotherapy. Our studies show that the TR-107 compound, an agonist of ClpP - the proteolytic subunit of mitochondrial maintenance complex - can synergize with Erastin, an inducer of ferroptosis cell death. TR-107 potently disrupts mitochondrial proteostasis and attenuates oxidative phosphorylation, resulting in excessive oxidative stress. Here, we show that Erastin synergizes with TR-107 activity by downregulating the cofac

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Frye, William J. E., Lyn M. Huff, José M. González Dalmasy, et al. "The multidrug resistance transporter P-glycoprotein confers resistance to ferroptosis inducers." Cancer Drug Resistance 6 (2023): 468–80. http://dx.doi.org/10.20517/cdr.2023.29.

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Aim: Ferroptosis is a non-apoptotic form of cell death caused by lethal lipid peroxidation. Several small molecule ferroptosis inducers (FINs) have been reported, yet little information is available regarding their interaction with the ATP-binding cassette (ABC) transporters P-glycoprotein (P-gp, ABCB1) and ABCG2. We thus sought to characterize the interactions of FINs with P-gp and ABCG2, which may provide information regarding oral bioavailability and brain penetration and predict drug-drug interactions. Methods: Cytotoxicity assays with ferroptosis-sensitive A673 cells transfected to expres

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Wu, Hongxia, and Aiwen Liu. "Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer." Journal of International Medical Research 49, no. 3 (2021): 030006052199618. http://dx.doi.org/10.1177/0300060521996183.

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Objectives Ferroptosis is caused by iron-dependent lipid peroxide accumulation, the sensitivity of which might be regulated by acyl-CoA synthetase long chain family member 4 (ACSL4). Non-small-cell lung cancer (NSCLC) can resist oxidative stress and reduce the sensitivity of tumor cells to ferroptosis by changing the expression of some proteins. Mechanisms involving ferroptosis sensitivity in NSCLC are not fully understood. Methods A dual-luciferase reporter assay was used to confirm a targeting relationship between long non-coding (lnc)RNA NEAT1 and ACSL4. Overexpression and silencing assays

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Smirnova, Yuliya D., Dominik Hanetseder, Lukas Derigo, et al. "Osteosarcoma Cells and Undifferentiated Human Mesenchymal Stromal Cells Are More Susceptible to Ferroptosis than Differentiated Human Mesenchymal Stromal Cells." Antioxidants 14, no. 2 (2025): 189. https://doi.org/10.3390/antiox14020189.

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Current research suggests that promoting ferroptosis, a non-apoptotic form of cell death, may be an effective therapy for osteosarcoma, while its inhibition could facilitate bone regeneration and prevent osteoporosis. Our objective was to investigate whether the susceptibility to and regulation of ferroptosis differ between undifferentiated (UBC) and differentiated (DBC) human bone marrow stromal cells, as well as human osteosarcoma cells (MG63). Ferroptosis was induced by either inhibiting glutathione peroxidase 4 (GPX4) using RSL3 or blocking all glutathione-dependent enzymes through inhibit

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An, Lifeng, Jingwen Huang, Shihui Ge, Xin Zhang, and Jing Wang. "lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma." Computational and Mathematical Methods in Medicine 2022 (June 6, 2022): 1–8. http://dx.doi.org/10.1155/2022/1972516.

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Long noncoding RNAs (lncRNAs) stand as indispensable regulators of initiation and development in melanoma (melanoma). However, the action molecular mechanisms linked to melanoma remain unclear. In the current study, the findings revealed that AGAP2-AS1 was considerably greater in melanoma than in healthy tissues and that the level of AGAP2-AS1 in cancer tissue was significantly linked to the cancerous TNM stage of patients. Individuals with high AGAP2-AS1 had a considerably shorter survival duration than patients with low AGAP2-AS1, regardless of progression-free survival or overall survival.

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Zhao, Chang, Guchun Qin, Caixia Ling, et al. "MSNs-loaded HMME and Erastin-mediated ferroptosis combined with sonodynamic therapy for HCC treatment." Journal of Cancer Research and Therapeutics 21, no. 2 (2025): 465–76. https://doi.org/10.4103/jcrt.jcrt_1531_24.

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ABSTRACT Background: Ferroptosis can have a major impact on the development and advancement of hepatocellular carcinoma (HCC) due to its clear association with heightened vulnerability to the disease. This study aimed to develop a novel nanoplatform to evaluate its effectiveness in in vivo and in vitro models of HCC. Methods: Erastin, a compound that induces iron-dependent cell death, and HMME, a sonosensitizer, were enclosed within mesoporous silica nanoparticles (MSNs). The nanoparticles were engineered to exhibit a responsive assembly-disassembly mechanism. Hydrophilic hyaluronic acid (HA)

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Fenniri, Zachariah A. H., Sarah Lane, Juergen Ehlting, and Patrick B. Walter. "Monocytic Leukemia Cell Resistance to Ferroptosis Is Overcome By Iron Chelation." Blood 144, Supplement 1 (2024): 7468. https://doi.org/10.1182/blood-2024-211689.

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Introduction:In the United States, acute myeloid leukemias (AML) have a mean 5-year survival rate of 32%, while the monocytic subtype (AMoL) has a mean 5-year survival rate of 27%1. Therapies targeting induction of ferroptosis hold promise as new strategies for AML, however, resistance can be a problem2. To investigate ferroptosis resistance, we have studied iron deficiency and excess in AMoL cells. Fundamentally it is problematic to have either too little iron (dysfunctional energy metabolism and DNA repair) or too much iron (increased reactive oxygen species (ROS) that induce ferroptosis). D

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Guo, Xinxin, Yubo Guo, Jiahuan Li, Qian Liu, and Hao Wu. "Arginine Expedites Erastin-Induced Ferroptosis through Fumarate." International Journal of Molecular Sciences 24, no. 19 (2023): 14595. http://dx.doi.org/10.3390/ijms241914595.

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Ferroptosis is a newly characterized form of programmed cell death. The fundamental biochemical feature of ferroptosis is the lethal accumulation of iron-catalyzed lipid peroxidation. It has gradually been recognized that ferroptosis is implicated in the pathogenesis of a variety of human diseases. Increasing evidence has shed light on ferroptosis regulation by amino acid metabolism. Herein, we report that arginine deprivation potently inhibits erastin-induced ferroptosis, but not RSL3-induced ferroptosis, in several types of mammalian cells. Arginine presence reduces the intracellular glutath

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Brown, Caitlin W., John J. Amante, Hira Lal Goel та Arthur M. Mercurio. "The α6β4 integrin promotes resistance to ferroptosis". Journal of Cell Biology 216, № 12 (2017): 4287–97. http://dx.doi.org/10.1083/jcb.201701136.

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Increases in lipid peroxidation can cause ferroptosis, a form of cell death triggered by inhibition of glutathione peroxidase 4 (GPX4), which catalyzes the reduction of lipid peroxides and is a target of ferroptosis inducers, such as erastin. The α6β4 integrin protects adherent epithelial and carcinoma cells from ferroptosis induced by erastin. In addition, extracellular matrix (ECM) detachment is a physiologic trigger of ferroptosis, which is evaded by α6β4. The mechanism that enables α6β4 to evade ferroptosis involves its ability to protect changes in membrane lipids that are proferroptotic.

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Li, Yaoqi, Xinyu Wang, Junjie Yan, et al. "Nanoparticle ferritin-bound erastin and rapamycin: a nanodrug combining autophagy and ferroptosis for anticancer therapy." Biomaterials Science 7, no. 9 (2019): 3779–87. http://dx.doi.org/10.1039/c9bm00653b.

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Lu, Ruiqing, Yinan Jiang, Xianxin Lai, Shujie Liu, Litao Sun, and Zhong-Wei Zhou. "A Shortage of FTH Induces ROS and Sensitizes RAS-Proficient Neuroblastoma N2A Cells to Ferroptosis." International Journal of Molecular Sciences 22, no. 16 (2021): 8898. http://dx.doi.org/10.3390/ijms22168898.

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Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, a common child malignant tumor with minimal treatment, is unclear. This study investigated the anti-cancer function of ferroptosis inducer Erastin or RSL3 in neuroblastoma N2A cells. Our results show that Erastin or RSL3 induces ROS level and cell death and, therefore, reduces the viability of RAS-proficient N2A cells. Importantly, inhibitors t

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Su, I.-Chang, Yu-Kai Su, Syahru Agung Setiawan, et al. "NADPH Oxidase Subunit CYBB Confers Chemotherapy and Ferroptosis Resistance in Mesenchymal Glioblastoma via Nrf2/SOD2 Modulation." International Journal of Molecular Sciences 24, no. 9 (2023): 7706. http://dx.doi.org/10.3390/ijms24097706.

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Glioblastoma multiforme (GBM) is a highly heterogeneous disease with a mesenchymal subtype tending to exhibit more aggressive and multitherapy-resistant features. Glioblastoma stem-cells derived from mesenchymal cells are reliant on iron supply, accumulated with high reactive oxygen species (ROS), and susceptible to ferroptosis. Temozolomide (TMZ) treatment is the mainstay drug for GBM despite the rapid development of resistance in mesenchymal GBM. The main interconnection between mesenchymal features, TMZ resistance, and ferroptosis are poorly understood. Herein, we demonstrated that a subuni

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Nagase, Haruna, Yasuhiro Katagiri, Kentaro Oh-hashi, Herbert M. Geller, and Yoko Hirata. "Reduced Sulfation Enhanced Oxytosis and Ferroptosis in Mouse Hippocampal HT22 Cells." Biomolecules 10, no. 1 (2020): 92. http://dx.doi.org/10.3390/biom10010092.

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Sulfation is a common modification of extracellular glycans, tyrosine residues on proteins, and steroid hormones, and is important in a wide variety of signaling pathways. We investigated the role of sulfation on endogenous oxidative stress, such as glutamate-induced oxytosis and erastin-induced ferroptosis, using mouse hippocampal HT22 cells. Sodium chlorate competitively inhibits the formation of 3′-phosphoadenosine 5′-phosphosulfate, the high energy sulfate donor in cellular sulfation reactions. The treatment of HT22 cells with sodium chlorate decreased sulfation of heparan sulfate proteogl

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El Hajj, Sarah, Laetitia Canabady-Rochelle, Isabelle Fries-Raeth, and Caroline Gaucher. "A Smooth Muscle Cell-Based Ferroptosis Model to Evaluate Iron-Chelating Molecules for Cardiovascular Disease Treatment." Current Issues in Molecular Biology 46, no. 2 (2024): 1348–59. http://dx.doi.org/10.3390/cimb46020086.

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Dysregulation of iron homeostasis causes iron-mediated cell death, recently described as ferroptosis. Ferroptosis is reported in many chronic diseases, such as hepatic cancer, renal, and cardiovascular diseases (heart failure, atherosclerosis). However, there is a notable scarcity of research studies in the existing literature that explore treatments capable of preventing ferroptosis. Additionally, as far as the author is aware, there is currently no established model for studying ferroptosis within cardiovascular cells, which would be essential for assessing metal-chelating molecules with the

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Bai, Yu-Ting, Rong Chang, Hua Wang, Feng-Jun Xiao, Ri-Li Ge, and Li-Sheng Wang. "ENPP2 protects cardiomyocytes from erastin-induced ferroptosis." Biochemical and Biophysical Research Communications 499, no. 1 (2018): 44–51. http://dx.doi.org/10.1016/j.bbrc.2018.03.113.

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Devericks, Emily, Michael F. Coleman, Hannah Malian, Violet Kiesel, Dorothy Teegarden, and Stephen D. Hursting. "Abstract 1627: Metabolic links between obesity and ferroptosis in a murine model of breast cancer." Cancer Research 82, no. 12_Supplement (2022): 1627. http://dx.doi.org/10.1158/1538-7445.am2022-1627.

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Abstract Background Obesity is an established risk factor for post-menopausal triple negative breast cancer (TNBC). Multiple aspects of fatty acid metabolism, including fatty acid synthesis, are upregulated in white adipose tissue during obesity development. The enzyme pyruvate carboxylase (PC), a supportive player in fatty acid synthesis, is relied upon for metastasis of murine TNBC particularly in models of obesity- further elucidating the importance of fatty acid metabolism to breast cancer progression in those with obesity. Ferroptosis, a method of cell death induced by peroxidation of pho

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Liu, Jiaxi, Rui Liu, Ru Zhang, et al. "Erastin Induces Ferrotposis in Multiple Myeloma Cells through SLC7A11-IRF1-Txn Axis." Blood 144, Supplement 1 (2024): 6853. https://doi.org/10.1182/blood-2024-209081.

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Introduction:Multiple myeloma (MM) is the second most common hematological malignancy characterized by genetic heterogeneity. Ferroptosis is a newly defined form of regulated cell death with promising antitumor results in some cancers, while the relationship between MM and ferroptosis remains largely unclear. One of the most important ferrotposis defence pathway is the SLC7A11-GSH-GPX4 axis, here we observed erastin inhibits thioredoxin(TXN) and finally lead to ferrotposis in MM cells. TXN as a essential oxidative stress molecular play a part in cellar pathways, but how it effects ferroptosis

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Li, Pengxiang, Xuefeng Lv, Lu Liu, Mengle Peng, and Dongchun Qin. "The Role of Ferroptosis-Related Molecules and Significance of Ferroptosis Score in Cervical Cancer." Journal of Oncology 2022 (October 30, 2022): 1–18. http://dx.doi.org/10.1155/2022/7835698.

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Background. Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, may be a potential treatment for many cancers, including cervical cancer (CC). However, the regulation of long noncoding RNAs (lncRNAs) in the process of ferroptosis and whether ferroptosis inducers could increase the cytotoxicity of conventional chemotherapy drugs remain to be further elucidated. Methods. We analyzed the variation of 55 differentially ferroptosis-related genes (FRGs) and the influence of mutations in CC patients. The patients with CC were classified into two ferroptosis clusters by the

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Xu, Chao, Su Ni, Nanwei Xu, et al. "Theaflavin-3,3 ′ -Digallate Inhibits Erastin-Induced Chondrocytes Ferroptosis via the Nrf2/GPX4 Signaling Pathway in Osteoarthritis." Oxidative Medicine and Cellular Longevity 2022 (November 17, 2022): 1–17. http://dx.doi.org/10.1155/2022/3531995.

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There is evidence that osteoarthritis (OA) is associated with ferroptosis which is a kind of lipid peroxidation-related cell death. Theaflavin-3,3 ′ -digallate(TF3), a polyphenol compound extracted from black tea, possesses antioxidative and anti-inflammatory properties, but its effects on chondrocyte ferroptosis in osteoarthritis (OA) remain unclear. Our present study aims at exploring the protective role and underlying mechanisms of TF3 against erastin-induced chondrocyte ferroptosis in OA. In human primary chondrocytes treated with erastin alone or combined with different doses of TF3, cell

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Kong, Enjun, Yan Xu, and Haichen Yang. "Total flavonoids of Rhizoma drynariae influence ferroptosis in osteoblasts via miR-205-5p/GPX4 axis." Tropical Journal of Pharmaceutical Research 22, no. 7 (2023): 1379–86. http://dx.doi.org/10.4314/tjpr.v22i7.4.

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Purpose: This research investigated the biological effects of total flavonoids of Rhizoma Drynariae (TFRD) on osteoporosis in mice.Methods: Mice were subjected to bilateral ovariectomy (OVX) to generate the osteoporosis model used, which was then intragastrically administered TFRD daily at a dose of 75 mg/kg. Bone loss was examined histologically using H&E staining. Moreover, erastin-treated primary osteoblasts were used to further analyze the effect of TFRD on ferroptosis. Reactive oxygen species (ROS), ferrous iron level, and CCK-8 method were employed to determine the protective influen

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Pinto-Junior, Vanir Reis, Rodrigo Lopes Seeger, Cláudio Henrique Dahne Souza-Filho, et al. "Xc- System as a Possible Target for ConBr Lectin Interaction in Glioma Cells." Neuroglia 5, no. 3 (2024): 202–22. http://dx.doi.org/10.3390/neuroglia5030015.

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Studies have revealed the dependence of glioma cells on iron, making them sensitive to ferroptosis. Ferroptosis can be triggered by inhibition of the xc- system, resulting in redox imbalance and membrane lipid peroxidation. The xc- system is composed of two coupled proteins, xCT and CD98hc. The control of transporters, such as xCT, by the CD98hc glycoprotein suggests that molecules targeting glycans may have an impact on the treatment of glioma. This study evaluated the effect of the Canavalia brasiliensis (ConBr) lectin on C6 glioma cells and compared it with erastin, an xc- system inhibitor.

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He, Weiwei, Wenying Shu, Lu Xue, et al. "Synergistic Effect of Erastin Combined with Nutlin-3 on Vestibular Schwannoma Cells as p53 Modulates Erastin-Induced Ferroptosis Response." Journal of Oncology 2022 (March 21, 2022): 1–18. http://dx.doi.org/10.1155/2022/7507857.

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Vestibular schwannoma (VS) is a rare neurotology neoplasm that results in partial neurological defects. As we know, a comprehensive understanding of basic mechanisms and targeted therapy is vital for disease management. In VS, p53 has been proved to suppress tumor progression via a cooperative with the key protein, merlin, as well as regulation of the cell cycle. However, there are more potential mechanisms of p53 in VS needed to exploit. First, via genome-wide RNA expression analysis, we identified differentially expressed genes in VS compared with normal nerves, and then, bioinformatics anal

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Lee, Namgyu, Anne E. Carlisle, Austin Peppers, et al. "xCT-Driven Expression of GPX4 Determines Sensitivity of Breast Cancer Cells to Ferroptosis Inducers." Antioxidants 10, no. 2 (2021): 317. http://dx.doi.org/10.3390/antiox10020317.

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Inducers of ferroptosis such as the glutathione depleting agent Erastin and the GPX4 inhibitor Rsl-3 are being actively explored as potential therapeutics in various cancers, but the factors that determine their sensitivity are poorly understood. Here, we show that expression levels of both subunits of the cystine/glutamate antiporter xCT determine the expression of GPX4 in breast cancer, and that upregulation of the xCT/selenocysteine biosynthesis/GPX4 production axis paradoxically renders the cancer cells more sensitive to certain types of ferroptotic stimuli. We find that GPX4 is strongly u

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Ouyang, Xiaojian, Xican Li, Jie Liu, et al. "Structure–activity relationship and mechanism of four monostilbenes with respect to ferroptosis inhibition." RSC Advances 10, no. 52 (2020): 31171–79. http://dx.doi.org/10.1039/d0ra04896h.

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Erastin-treated bone marrow-derived mesenchymal stem cells (bmMSCs) were prepared and used to compare the ferroptosis inhibitory bioactivities of four monostilbenes, including rhapontigenin (1a), isorhapontigenin (1b), piceatannol-3′-O-glucoside (1c), and rhapontin (1d).

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Meier, Julia K., Matthias Schnetz, Susanne Beck, et al. "Iron-Bound Lipocalin-2 Protects Renal Cell Carcinoma from Ferroptosis." Metabolites 11, no. 5 (2021): 329. http://dx.doi.org/10.3390/metabo11050329.

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While the importance of the iron-load of lipocalin-2 (Lcn-2) in promoting tumor progression is widely appreciated, underlying molecular mechanisms largely remain elusive. Considering its role as an iron-transporter, we aimed at clarifying iron-loaded, holo-Lcn-2 (hLcn-2)-dependent signaling pathways in affecting renal cancer cell viability. Applying RNA sequencing analysis in renal CAKI1 tumor cells to explore highly upregulated molecular signatures in response to hLcn-2, we identified a cluster of genes (SLC7A11, GCLM, GLS), which are implicated in regulating ferroptosis. Indeed, hLcn-2-stimu

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Li, Yichen, Xing Wang, Yong-Hua Chen, Qing-Quan Tan, Xu-Bao Liu, and Chunlu Tan. "Clusterin is upregulated by erastin, a ferroptosis inducer and exerts cytoprotective effects in pancreatic adenocarcinoma cells." Anti-Cancer Drugs, December 13, 2023. http://dx.doi.org/10.1097/cad.0000000000001561.

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Ferroptosis is a novel form of cell death, which is distinguished from apoptosis and necrosis, and characterized by accumulation of lipid-based reactive oxygen species (ROS) in an iron-dependent manner. Erastin, a small molecule, was widely reported to trigger ferroptosis in various kinds of cancer cells, including pancreatic cancer cells by inducing ROS accumulation. However, how erastin treatment exerts cytotoxicity is not still fully understood. In this study, the effects of erastin in causing pancreatic cancer cell death via inducing ferroptosis and apoptosis are investigated. As expected,

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Li, Yajie, Xinliu Zeng, Dingheng Lu, Minuo Yin, Meirong Shan, and Ying Gao. "Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis." Human Reproduction, December 30, 2020. http://dx.doi.org/10.1093/humrep/deaa363.

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Abstract STUDY QUESTION Could erastin activate ferroptosis to regress endometriotic lesions? SUMMARY ANSWER Erastin could induce ferroptosis to regress endometriotic lesions in endometriosis. WHAT IS KNOWN ALREADY Ectopic endometrial stromal cells (EESCs) are in an iron overloading microenvironment and tend to be more sensitive to oxidative damage. The feature of erastin-induced ferroptosis is iron-dependent accumulation of lethal lipid reactive oxygen species (ROS). STUDY DESIGN, SIZE, DURATION Eleven patients without endometriosis and 21 patients with endometriosis were recruited in this stu

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Wu, Xiangping, and Jing Wu. "A polo-like kinase 1 inhibitor enhances erastin sensitivity in head and neck squamous cell carcinoma cells in vitro." Cancer Chemotherapy and Pharmacology, March 27, 2024. http://dx.doi.org/10.1007/s00280-024-04654-8.

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Abstract Background Polo-like kinase 1 (PLK1) is a critical therapeutic target in the treatment of head and neck squamous cell carcinoma (HNSCC). The objective of this study was to investigate the therapeutic effect of the combination of BI 2536, a PLK1 inhibitor, and erastin, a ferroptosis inducer, in HNSCC. Methods The proliferation, invasion, and migration abilities of Tu177 and FaDu cells upon exposure to BI 2536 and erastin, used in combination or alone, were tested. Fe2+, glutathione (GSH), and malondialdehyde (MDA) detection kits were used to determine whether the addition of BI 2536 en

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Chen, Fangfang, Shiqi Wu, Ni Kuang, Yan Zeng, Meixi Li, and Chen Xu. "ABCB1‐mediated docetaxel resistance reversed by erastin in prostate cancer." FEBS Journal, May 7, 2024. http://dx.doi.org/10.1111/febs.17135.

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Docetaxel (Doc) currently serves as the primary first‐line treatment for patients with castrate‐resistant prostate cancer (CRPC). Erastin, a small molecule compound, can trigger inhibition of the cystine–glutamate reverse transport system and other pathways, leading to iron‐dependent cell death (ferroptosis). Beyond its role in inducing cancer cell death, erastin demonstrates potential when combined with chemotherapy drugs to heighten cancer cell drug susceptibility. However, the augmentation by erastin of the effects of Doc treatment on prostate cancer, and the underlying mechanisms involved,

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