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Journal articles on the topic 'System xc - antiporter'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Dhaval, V. Patel Mukesh Nandave Prashant S. Kharkar. "PHARMACOPHORE MODELLING FOR THE DISCOVERY OF SYSTEM XC- ANTIPORTER INHIBITORS." INDO AMERICAN JOURNAL OF PHARMACEUTICAL RESEARCH 07, no. 09 (2017): 532–36. https://doi.org/10.5281/zenodo.1036492.

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Cancer is one of the major disorders with increasing rates of morbidity and mortality. Recent drug discovery of anti cancer drug has identified several molecular targets and tried to achieve a goal of therapeutic effecative and safe molecule. Amongst these, system xc- antiporter is a novel promising target to control cancer progression. This antiporter is found to be over expressed in majority of cancer cells and functions by transporting amino acids, cystine and glutamate, in opposite directions. System xc- antiporter uptakes one molecule of cystine with the release of one molecule of glutama

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Martis, Renita M., Luis J. Knight, Paul J. Donaldson, and Julie C. Lim. "Identification, Expression, and Roles of the Cystine/Glutamate Antiporter in Ocular Tissues." Oxidative Medicine and Cellular Longevity 2020 (June 18, 2020): 1–10. http://dx.doi.org/10.1155/2020/4594606.

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The cystine/glutamate antiporter (system xc-) is composed of a heavy chain subunit 4F2hc linked by a disulphide bond to a light chain xCT, which exchanges extracellular cystine, the disulphide form of the amino acid cysteine, for intracellular glutamate. In vitro research in the brain, kidney, and liver have shown this antiporter to play a role in minimising oxidative stress by providing a source of intracellular cysteine for the synthesis of the antioxidant glutathione. In vivo studies using the xCT knockout mouse revealed that the plasma cystine/cysteine redox couple was tilted to a more oxi

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Hung, Chung-Chieh, Chieh-Hsin Lin, and Hsien-Yuan Lane. "Cystine/Glutamate Antiporter in Schizophrenia: From Molecular Mechanism to Novel Biomarker and Treatment." International Journal of Molecular Sciences 22, no. 18 (2021): 9718. http://dx.doi.org/10.3390/ijms22189718.

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Glutamate, a crucial excitatory neurotransmitter, plays a major role in the modulation of schizophrenia’s pathogenesis. New drug developments for schizophrenia have been prompted by the hypoglutamatergic hypothesis of schizophrenia. The cystine/glutamate antiporter system xc− is related to glutamate-release regulation. Patients with schizophrenia were recently discovered to exhibit downregulation of xc− subunits—the solute carrier (SLC) family 3 member 2 and the SLC family 7 member 11. We searched for relevant studies from 1980, when Bannai and Kitamura first identified the protein subunit sys

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de Baat, Axel, Daniel T. Meier, Adriano Fontana, Marianne Böni-Schnetzler, and Marc Y. Donath. "Cystine/Glutamate antiporter system xc- deficiency impairs macrophage glutathione metabolism and cytokine production." PLOS ONE 18, no. 10 (2023): e0291950. http://dx.doi.org/10.1371/journal.pone.0291950.

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System xc-, encoded by Slc7a11, is an antiporter responsible for exporting glutamate while importing cystine, which is essential for protein synthesis and the formation of thiol peptides, such as glutathione. Glutathione acts as a co-factor for enzymes responsible for scavenging reactive oxygen species. Upon exposure to bacterial products, macrophages exhibit a rapid upregulation of system xc-. This study investigates the impact of Slc7a11 deficiency on the functionality of peritoneal and bone marrow-derived macrophages. Our findings reveal that the absence of Slc7a11 results in significantly

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5

Domercq, M., B. Szczupak, J. Gejo, et al. "PET imaging with [18F]FSPG evidences the role of system xc- on brain inflammation following cerebral ischemia in rats." Theranostics 6, no. 11 (2016): 1753–67. https://doi.org/10.7150/thno.15616.

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In vivo Positron Emission Tomography (PET) imaging of the cystine-glutamate antiporter (system xc-) activity with [18F]FSPG is meant to be an attractive tool for the diagnosis and therapy evaluation of brain diseases. However, the role of system xc- in cerebral ischemia and its involvement in inflammatory reaction has been scarcely explored. In this work, we report the longitudinal investigation of the neuroinflammatory process following transient middle cerebral artery occlusion (MCAO) in rats using PET with [18F]FSPG and the translocator protein (TSPO) ligand [18F]DPA-714. In the ischemic te

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6

Wang, Weimin, Michael Green, Jae Eun Choi, et al. "CD8+ T cells regulate tumor ferroptosis by targeting the system xc− during cancer immunotherapy." Journal of Immunology 202, no. 1_Supplement (2019): 137.11. http://dx.doi.org/10.4049/jimmunol.202.supp.137.11.

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Abstract Cytotoxic T cells recognize specific antigens expressed on tumor cells and mediate tumor cell apoptosis mainly through perforin–granzyme-mediated and FAS-mediated pathways. Ferroptosis is a recently discovered form of cell death that differs from apoptosis and results from iron-dependent lipid peroxide accumulation. The potential contribution of CD8+ T cell-mediated cytotoxic activity and immunotherapy to tumor ferroptosis remains unknown. Here, we find that immunotherapy-activated CD8+ T cells sensitize tumor cell ferroptosis. Mechanistically, IFNγ released from CD8+ T cells downregu

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7

Yoon, Sang Jun, and Gina M. DeNicola. "IL1RAP Pulls a Double Shift in the Cysteine Factory." Cancer Discovery 11, no. 11 (2021): 2679–81. http://dx.doi.org/10.1158/2159-8290.cd-21-1053.

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Abstract Summary: Anoikis is a critical barrier to cancer cell metastasis. In this issue of Cancer Discovery, Zhang and colleagues identify that IL1 receptor accessory protein suppresses anoikis in Ewing sarcoma by promoting both the activity of the system Xc− cystine/glutamate antiporter and cystathionine γ-lyase (CTH) transcription to sustain cysteine levels for reactive oxygen species detoxification. See related article by Zhang et al., p. 2884.

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8

Gallagher, Martin. "The System xc- Cystine/Glutamate Antiporter: An Exciting Target for Antiepileptogenic Therapy?" Epilepsy Currents 20, no. 1 (2020): 39–42. http://dx.doi.org/10.1177/1535759719891983.

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9

Rebalka, Irena A., Andrew W. Cao, Linda L. May, Mark A. Tarnopolsky, and Thomas J. Hawke. "Statin administration activates system xC− in skeletal muscle: a potential mechanism explaining statin-induced muscle pain." American Journal of Physiology-Cell Physiology 317, no. 5 (2019): C894—C899. http://dx.doi.org/10.1152/ajpcell.00308.2019.

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Statins are a cholesterol-lowering drug class that significantly reduce cardiovascular disease risk. Despite their safety and effectiveness, musculoskeletal side-effects, particularly myalgia, are prominent and the most common reason for discontinuance. The cause of statin-induced myalgia is unknown, so defining the underlying mechanism(s) and potential therapeutic strategies is of clinical importance. Here we tested the hypothesis that statin administration activates skeletal muscle system xC−, a cystine/glutamate antiporter, to increase intracellular cysteine and therefore glutathione synthe

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10

Zhang, Lei, Wen Liu, Fangyan Liu, et al. "IMCA Induces Ferroptosis Mediated by SLC7A11 through the AMPK/mTOR Pathway in Colorectal Cancer." Oxidative Medicine and Cellular Longevity 2020 (April 4, 2020): 1–14. http://dx.doi.org/10.1155/2020/1675613.

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Ferroptosis, implicated in several diseases, is a new form of programmed and nonapoptotic cell death triggered by iron-dependent lipid peroxidation after inactivation of the cystine/glutamate antiporter system xc–, which is composed of solute carrier family 7 membrane 11 (SLC7A11) and solute carrier family 3 membrane 2 (SLC3A2). Therefore, inducing ferroptosis through inhibiting the cystine/glutamate antiporter system xc– may be an effective way to treat cancer. In previous screening tests, we found that the benzopyran derivative 2-imino-6-methoxy-2H-chromene-3-carbothioamide (IMCA) significan

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Ma, Zhongping, and Qishan Ran. "Biological Functions and Therapeutic Potential of SLC7A11 Across Diseases." International Journal of Biology and Life Sciences 10, no. 3 (2025): 60–65. https://doi.org/10.54097/8907kw46.

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SLC7A11, a key component of the cystine/glutamate antiporter System Xc⁻, regulates redox balance and ferroptosis. Its dysregulation is linked to cancer, metabolic, neurodegenerative, immune, and kidney diseases. In tumors, SLC7A11 promotes growth and therapy resistance, while in non-cancerous tissues, it offers antioxidant protection. This review outlines the biological functions of SLC7A11, its dual disease roles, and therapeutic strategies including small molecule inhibitors, exosome delivery, and metabolic interventions. Though promising, clinical translation faces challenges in tissue spec

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12

Huang, Chao-Yuan, Li-Ju Chen, Grace Chen, Tzu-I. Chao, and Cheng-Yi Wang. "SHP-1/STAT3-Signaling-Axis-Regulated Coupling between BECN1 and SLC7A11 Contributes to Sorafenib-Induced Ferroptosis in Hepatocellular Carcinoma." International Journal of Molecular Sciences 23, no. 19 (2022): 11092. http://dx.doi.org/10.3390/ijms231911092.

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Ferroptosis is a type of iron-dependent cell death pertaining to an excess of lipid peroxidation. It has been suggested that sorafenib—an anti-angiogenic medication for hepatocellular carcinoma (HCC)—induces ferroptosis, but the underlying mechanism for this remains largely unknown. We employed siRNA-mediated gene silencing to investigate the role of Src homology region 2 domain-containing phosphatase-1 (SHP-1), following sorafenib treatment, in cystine/glutamate-antiporter-system-Xc−-regulated cystine uptake. Co-immunoprecipitation was also performed to examine the interactions between MCL1,

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13

Aboushousha, Reem, Jos van der Velden, Nicholas Hamilton, et al. "Abstract 1510: Glutathione-oxidation of ovarian tumor deubiquitinase-1 promotes lung adenocarcinoma survival through stabilizing system xc-." Cancer Research 85, no. 8_Supplement_1 (2025): 1510. https://doi.org/10.1158/1538-7445.am2025-1510.

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Abstract The small thiol antioxidant glutathione (GSH) is critical in maintaining redox homeostasis that is essential in combating oxidative stress. We and others have reported increases of GSH in KRAS-mutant lung adenocarcinoma (LUAD). However, little is known about GSH-dependent protein oxidation (S-glutathionylation- PSSG) in LUAD development and progression. We recently discovered that glutaredoxin (GLRX), the enzyme that reverses PSSG, is decreased in human LUAD, and that KrasG12D-induced lung tumorigenesis is enhanced in mice lacking Glrx. To elucidate the link between PSSG and GSH level

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14

Nakano, Tomosuke, Toshiki Hasegawa, Dai Suzuki, Eishi Motomura, and Motohiro Okada. "Amantadine Combines Astroglial System Xc− Activation with Glutamate/NMDA Receptor Inhibition." Biomolecules 9, no. 5 (2019): 191. http://dx.doi.org/10.3390/biom9050191.

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A glutamate/NMDA receptor (NMDA-R) antagonist, amantadine (AMA) exhibits a broad spectrum of clinically important properties, including antiviral, antiparkinsonian, neuroprotective, neuro-reparative and cognitive-enhancing effects. However, both clinical and pre-clinical studies have demonstrated that noncompetitive NMDA-R antagonists induce severe schizophrenia-like cognitive deficits. Therefore, this study aims to clarify the clinical discrepancy between AMA and noncompetitive NMDA-R antagonists by comparing the effects of AMA with those of a noncompetitive NMDA-R antagonist, MK801, on rat t

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15

Bridges, Richard J., Nicholas R. Natale, and Sarjubhai A. Patel. "System xc- cystine/glutamate antiporter: an update on molecular pharmacology and roles within the CNS." British Journal of Pharmacology 165, no. 1 (2011): 20–34. http://dx.doi.org/10.1111/j.1476-5381.2011.01480.x.

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16

Takeuchi, Satoru, Kojiro Wada, Terushige Toyooka, et al. "Increased xCT Expression Correlates With Tumor Invasion and Outcome in Patients With Glioblastomas." Neurosurgery 72, no. 1 (2012): 33–41. http://dx.doi.org/10.1227/neu.0b013e318276b2de.

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Abstract BACKGROUND: xCT is a light chain of the cystine/glutamate antiporter system xc−. Glutamate that is released by system xc− plays an important role in the infiltration of glioblastoma (GBM) cells. Furthermore, increased glutathione synthesis by system xc− may protect tumor cells against oxidative stress induced by radiotherapy and chemotherapy. OBJECTIVE: To investigate whether the levels of xCT expression correlated with infiltrative imaging phenotypes on magnetic resonance imaging and outcomes in patients with GBMs. METHODS: Forty patients with histologically confirmed primary GBMs we

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17

Ianiro, Giusi, Veronica D’Ezio, Ludovica Carpinelli, et al. "Iron Saturation Drives Lactoferrin Effects on Oxidative Stress and Neurotoxicity Induced by HIV-1 Tat." International Journal of Molecular Sciences 24, no. 9 (2023): 7947. http://dx.doi.org/10.3390/ijms24097947.

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The Trans-Activator of Transcription (Tat) of Human Immunodeficiency Virus (HIV-1) is involved in virus replication and infection and can promote oxidative stress in human astroglial cells. In response, host cells activate transcription of antioxidant genes, including a subunit of System Xc− cystine/glutamate antiporter which, in turn, can trigger glutamate-mediated excitotoxicity. Here, we present data on the efficacy of bovine Lactoferrin (bLf), both in its native (Nat-bLf) and iron-saturated (Holo-bLf) forms, in counteracting oxidative stress in U373 human astroglial cells constitutively ex

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18

Shi, Jingxue, Yan He, Sandra J. Hewett та James A. Hewett. "Interleukin 1β Regulation of the System xc− Substrate-specific Subunit, xCT, in Primary Mouse Astrocytes Involves the RNA-binding Protein HuR". Journal of Biological Chemistry 291, № 4 (2015): 1643–51. http://dx.doi.org/10.1074/jbc.m115.697821.

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System xc− is a heteromeric amino acid cystine/glutamate antiporter that is constitutively expressed by cells of the CNS, where it functions in the maintenance of intracellular glutathione and extracellular glutamate levels. We recently determined that the cytokine, IL-1β, increases the activity of system xc− in CNS astrocytes secondary to an up-regulation of its substrate-specific light chain, xCT, and that this occurs, in part, at the level of transcription. However, an in silico analysis of the murine xCT 3′-UTR identified numerous copies of adenine- and uridine-rich elements, raising the p

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19

Kolb, A., S. Piccirillo, and C. Watts. "P49 * SENSITIZING GLIOBLASTOMA CELLS TO THERAPY BY TARGETING THE L-GLUTAMATE/L-CYSTINE ANTIPORTER SYSTEM XC-." Neuro-Oncology 16, suppl 6 (2014): vi8. http://dx.doi.org/10.1093/neuonc/nou249.37.

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20

Lewerenz, Jan, Mathias Klein, and Axel Methner. "Cooperative action of glutamate transporters and cystine/glutamate antiporter system Xc- protects from oxidative glutamate toxicity." Journal of Neurochemistry 98, no. 3 (2006): 916–25. http://dx.doi.org/10.1111/j.1471-4159.2006.03921.x.

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21

Wu, X. "EP22.25: Ultrasonic cavitation inhibits the antiporter system Xc‐ to promote ferroptosis in paclitaxel‐resistant ovarian cancer." Ultrasound in Obstetrics & Gynecology 64, S1 (2024): 324–25. http://dx.doi.org/10.1002/uog.28914.

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Kolb, A. K., S. Piccirillo, and C. Watts. "P03.04 * SENSITIZING GLIOBLASTOMA CELLS TO THERAPY BY TARGETING THE L-GLUTAMATE/L-CYSTINE ANTIPORTER SYSTEM XC-." Neuro-Oncology 16, suppl 2 (2014): ii34—ii35. http://dx.doi.org/10.1093/neuonc/nou174.127.

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23

Mawatari, K., Y. Yasui, K. Sugitani, T. Takadera, and S. Kato. "Reactive oxygen species involved in the glutamate toxicity of C6 glioma cells via XC¯ antiporter system." Neuroscience 73, no. 1 (1996): 201–8. http://dx.doi.org/10.1016/0306-4522(96)00025-5.

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24

Albrecht, Philipp, Jan Lewerenz, Sonja Dittmer, Rebecca Noack, Pamela Maher, and Axel Methner. "Mechanisms of Oxidative Glutamate Toxicity: The Glutamate/Cystine Antiporter System xc¯ as a Neuroprotective Drug Target." CNS & Neurological Disorders - Drug Targets 9, no. 3 (2010): 373–82. http://dx.doi.org/10.2174/187152710791292567.

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25

Slosky, Lauren M., Neemah M. BassiriRad, Ashley M. Symons, et al. "The cystine/glutamate antiporter system xc− drives breast tumor cell glutamate release and cancer-induced bone pain." PAIN 157, no. 11 (2016): 2605–16. http://dx.doi.org/10.1097/j.pain.0000000000000681.

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Lewerenz, Jan, Sandra J. Hewett, Ying Huang, et al. "The Cystine/Glutamate Antiporter System xc− in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities." Antioxidants & Redox Signaling 18, no. 5 (2013): 522–55. http://dx.doi.org/10.1089/ars.2011.4391.

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Slosky, L., N. BassiriRad, A. Symons-Liguori, et al. "(277) The cystine-glutamate antiporter system xc- drives tumor cell glutamate release and cancer-induced bone pain." Journal of Pain 16, no. 4 (2015): S45. http://dx.doi.org/10.1016/j.jpain.2015.01.195.

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28

Bauer, Georg. "Inhibition of Membrane-Associated Catalase, Extracellular ROS/RNS Signaling and Aquaporin/H2O2-Mediated Intracellular Glutathione Depletion Cooperate during Apoptosis Induction in the Human Gastric Carcinoma Cell Line MKN-45." Antioxidants 10, no. 10 (2021): 1585. http://dx.doi.org/10.3390/antiox10101585.

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The human gastric carcinoma cell line MKN-45 is a prototype of bona fide tumor cells, as it is protected from the NADPH oxidase-1 (NOX-1)-driven HOCl- and nitric oxide (NO)/peroxynitrite apoptosis-inducing signaling pathways by a membrane-associated catalase. The use of inhibitors/scavengers shows that inhibition of membrane-associated catalase is sufficient for the activation of NO/peroxynitrite or HOCl signaling. However, this signaling is not sufficient for apoptosis induction, as intracellular glutathione peroxidase/glutathione counteracts these signaling effects. Therefore, intrusion of e

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Luo, Yusong, Guopeng Tian, Xiang Fang, Shengwei Bai, Guoqiang Yuan, and Yawen Pan. "Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities." Antioxidants 11, no. 11 (2022): 2123. http://dx.doi.org/10.3390/antiox11112123.

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Glioma is the most common intracranial malignant tumor, and the current main standard treatment option is a combination of tumor surgical resection, chemotherapy and radiotherapy. Due to the terribly poor five-year survival rate of patients with gliomas and the high recurrence rate of gliomas, some new and efficient therapeutic strategies are expected. Recently, ferroptosis, as a new form of cell death, has played a significant role in the treatment of gliomas. Specifically, studies have revealed key processes of ferroptosis, including iron overload in cells, occurrence of lipid peroxidation,

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Li, Yan, Zhibing Tan, Zhigang Li, Zhongsheng Sun, Shumin Duan, and Wei Li. "Impaired long-term potentiation and long-term memory deficits in xCT-deficient sut mice." Bioscience Reports 32, no. 3 (2012): 315–21. http://dx.doi.org/10.1042/bsr20110107.

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xCT is the functional subunit of the cystine/glutamate antiporter system xc−, which exchanges intracellular glutamate with extracellular cystine. xCT has been reported to play roles in the maintenance of intracellular redox and ambient extracellular glutamate, which may affect neuronal function. To assess a potential role of xCT in the mouse hippocampus, we performed fear conditioning and passive avoidance for long-term memories and examined hippocampal synaptic plasticity in wild-type mice and xCT-null mutants, sut mice. Long-term memory was impaired in sut mice. Normal basal synaptic transmi

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Fantone, Sonia, Federica Piani, Fabiola Olivieri, et al. "Role of SLC7A11/xCT in Ovarian Cancer." International Journal of Molecular Sciences 25, no. 1 (2024): 587. http://dx.doi.org/10.3390/ijms25010587.

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Ovarian cancer is one of the most dangerous gynecologic cancers worldwide and has a high fatality rate due to diagnosis at an advanced stage of the disease as well as a high recurrence rate due to the occurrence of chemotherapy resistance. In fact, chemoresistance weakens the therapeutic effects, worsening the outcome of this pathology. Solute Carrier Family 7 Member 11 (SLC7A11, also known as xCT) is the functional subunit of the Xc− system, an anionic L-cystine/L-glutamate antiporter expressed on the cell surface. SLC7A11 expression is significantly upregulated in several types of cancers in

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Uriach Dasca, Julia, Samuel Marashli, Eric C. Holland, Michael Weller, and Hans-Georg Wirsching. "EXTH-35. REPURPOSING OF CLINICALLY APPROVED GLUTAMATE ANTAGONISTS TO TREAT GLIOBLASTOMA." Neuro-Oncology 26, Supplement_8 (2024): viii244. http://dx.doi.org/10.1093/neuonc/noae165.0966.

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Abstract The neurotransmitter glutamate plays a fundamental role in promoting epilepsy and tumor progression in glioblastoma. Glioblastoma cells secrete glutamate into the tumor microenvironment via the cystine-glutamate antiporter system Xc, leading to neuronal hyperexcitability, excitotoxicity, and tumor cell invasion. Additionally, glutamatergic neuroglioma synapses drive glioma progression in preclinical tumor models. To pharmacologically counteract effects of glutamate in glioblastoma, we employed a triple combination of anti-glutamatergic drugs: gabapentin, sulfasalazine, and memantine,

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Čolović, Milena, Etienne Rousseau, Zhengxing Zhang, et al. "Synthesis and evaluation of an 18F-labeled boramino acid analog of aminosuberic acid for PET imaging of the antiporter system xC−." Bioorganic & Medicinal Chemistry Letters 28, no. 22 (2018): 3579–84. http://dx.doi.org/10.1016/j.bmcl.2018.06.014.

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Kanno, Hitomi, Zenji Kawakami, Kazushige Mizoguchi, Yasushi Ikarashi, and Yoshio Kase. "Yokukansan, a Kampo Medicine, Protects PC12 Cells from Glutamate-Induced Death by Augmenting Gene Expression of Cystine/Glutamate Antiporter System Xc−." PLoS ONE 9, no. 12 (2014): e116275. http://dx.doi.org/10.1371/journal.pone.0116275.

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Zhao, Yantao, Yunxia Du, Yijie Gao, Zhijie Xu, Dexiang Zhao, and Maowei Yang. "ATF3 Regulates Osteogenic Function by Mediating Osteoblast Ferroptosis in Type 2 Diabetic Osteoporosis." Disease Markers 2022 (October 26, 2022): 1–17. http://dx.doi.org/10.1155/2022/9872243.

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Purpose. Osteoporosis is a complication of type 2 diabetes, and it is characterized by reduced bone mass, augmented bone fragility, and increased risk of fracture, thus reducing patient quality of life, especially in the elderly. Ferroptosis has been implicated in the pathological process of type 2 diabetic osteoporosis (T2DOP), but the specific underlying mechanisms remain largely unknown. This study clarified the role of activating transcription factor 3 (ATF3) in T2DOP and explored its specific regulatory mechanism, providing a new treatment target for T2DOP. Methods. We cultured hFob1.19 c

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Kudryashova, Olga M., Alexey M. Nesterenko, Dmitry A. Korzhenevskii, et al. "Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis." Data 8, no. 7 (2023): 119. http://dx.doi.org/10.3390/data8070119.

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Ferroptosis is a unique variety of non-apoptotic cell death, driven by massive lipid oxidation in an iron-dependent manner. Since ferroptosis was introduced as a concept in 2012, it has demonstrated its essential role in the pathogenesis in neurodegenerative diseases and an important role in therapy-resistant cancer cells. Thus, detailed molecular understanding of both canonical and alternative ferroptosis pathways is required. There is a set of widely used chemical agents to modulate ferroptosis using different pathway targets: erastin blocks cystine–glutamate antiporter, system xc-; ML210 di

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Xia, Jun, Stephanie Sun, Matthew RM Jotte, et al. "Combined Inhibition of CXCR4 Signaling and System xc- Transporter Activity Induces Synthetic Lethality in T-ALL Cells By Suppressing Gsh and Inducing Ferroptosis." Blood 136, Supplement 1 (2020): 37. http://dx.doi.org/10.1182/blood-2020-142735.

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T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy that accounts for 10-15% of pediatric and 25% of adult ALL cases. Prior studies have established that most cases pf T-ALL are addicted to CXCR4 signaling. Indeed, strong preclinical data demonstrating therapeutic activity of BL-8040, a potent CXCR4 antagonist, have led to a clinical trial of BL-8040 in combination with nelarabine for patients with relapsed/refractory T-ALL (NCT02763384). However, the molecular mechanisms by which CXCR4 blockade induces T-ALL cell death are unknown. Using a human T-ALL xenotrans

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Bridges, Richard, Victoria Lutgen, Doug Lobner, and David A. Baker. "Thinking Outside the Cleft to Understand Synaptic Activity: Contribution of the Cystine-Glutamate Antiporter (System xc−) to Normal and Pathological Glutamatergic Signaling." Pharmacological Reviews 64, no. 3 (2012): 780–802. http://dx.doi.org/10.1124/pr.110.003889.

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Rohan Pal, Snehasis Jana, Nidhi Shree, Golam Sanjari Mondal, Rounak Seal, and Arin Bhattacharjee. "Ferroptosis: A unique form of iron-dependent regulated cell death and its role in different diseases." World Journal of Biology Pharmacy and Health Sciences 12, no. 3 (2022): 224–38. http://dx.doi.org/10.30574/wjbphs.2022.12.3.0249.

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Ferroptosis, a unique, non-apoptotic, iron-dependent, controlled cell death associated with excessive iron accumulation and phospholipid peroxidation. It causes a reduction in cell volume and an increased density of the mitochondrial membrane. This form of controlled cell death is genetically, biochemically, and morphologically unique from other cell deaths, such as apoptosis, uncontrolled necrosis, and necroptosis. Directly or indirectly, alteration of glutathione peroxidase by ferroptosis inducers, through various mechanisms, causes a loss of antioxidant potential and a build-up of lipid rea

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Fernández-Acosta, Roberto, Behrouz Hassannia, Jurgen Caroen, et al. "Molecular Mechanisms of Nemorosone-Induced Ferroptosis in Cancer Cells." Cells 12, no. 5 (2023): 735. http://dx.doi.org/10.3390/cells12050735.

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Ferroptosis is an iron-dependent cell death-driven by excessive peroxidation of polyunsaturated fatty acids (PUFAs) of membranes. A growing body of evidence suggests the induction of ferroptosis as a cutting-edge strategy in cancer treatment research. Despite the essential role of mitochondria in cellular metabolism, bioenergetics, and cell death, their function in ferroptosis is still poorly understood. Recently, mitochondria were elucidated as an important component in cysteine-deprivation-induced (CDI) ferroptosis, which provides novel targets in the search for new ferroptosis-inducing comp

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Rohan, Pal, Jana Snehasis, Shree Nidhi, Sanjari Mondal Golam, Seal Rounak, and Bhattacharjee Arin. "Ferroptosis: A unique form of iron-dependent regulated cell death and its role in different diseases." World Journal of Biology Pharmacy and Health Sciences 12, no. 3 (2022): 224–38. https://doi.org/10.5281/zenodo.7639064.

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Ferroptosis, a unique, non-apoptotic, iron-dependent, controlled cell death associated with excessive iron accumulation and phospholipid peroxidation. It causes a reduction in cell volume and an increased density of the mitochondrial membrane. This form of controlled cell death is genetically, biochemically, and morphologically unique from other cell deaths, such as apoptosis, uncontrolled necrosis, and necroptosis. Directly or indirectly, alteration of glutathione peroxidase by ferroptosis inducers, through various mechanisms, causes a loss of antioxidant potential and a build-up of lipid rea

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Choi, Jangmi, Min-Ho Park, Seok-Ho Shin, et al. "Quantification and Metabolite Identification of Sulfasalazine in Mouse Brain and Plasma Using Quadrupole-Time-of-Flight Mass Spectrometry." Molecules 26, no. 4 (2021): 1179. http://dx.doi.org/10.3390/molecules26041179.

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Sulfasalazine (SAS), an anti-inflammatory drug with potent cysteine/glutamate antiporter system xc-(SXC) inhibition has recently shown beneficial effects in brain-related diseases. Despite many reports related to central nervous system (CNS) effect of SAS, pharmacokinetics (PK) and metabolite identification studies in the brain for SAS were quite limited. The aim of this study was to investigate the pharmacokinetics and metabolite identification of SAS and their distributions in mouse brain. Using in vivo brain exposure studies (neuro PK), the PK parameters of SAS was calculated for plasma as

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Fratta Pasini, Anna Maria, Chiara Stranieri, Domenico Girelli, Fabiana Busti, and Luciano Cominacini. "Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?" Antioxidants 10, no. 11 (2021): 1677. http://dx.doi.org/10.3390/antiox10111677.

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Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the

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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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Chen, Juan, Donglai Ma, Jun Bao, Ying Zhang, and Guoxing Deng. "Roots of Astragalus propinquus Schischkin Regulate Transmembrane Iron Transport and Ferroptosis to Improve Cerebral Ischemia-Reperfusion Injury." Evidence-Based Complementary and Alternative Medicine 2022 (August 2, 2022): 1–16. http://dx.doi.org/10.1155/2022/7410865.

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Background. The dried roots of the Astragalus propinquus Schischkin (RAP) plant, as a traditional Chinese medicine, has been widely used to treat stroke, cerebral ischemia, qi deficiency, and hypertension. Buyang Huanwu decoction is traditionally used to treat stroke in China for more than 200 years and has a significant effect on cerebral ischemia, and RAP is monarch medicine of Buyang Huanwu decoction. Therefore, this study was designed to observe the regulatory effect of RAP on transmembrane iron transporters and ferroptosis-related factors in cerebral ischemia-reperfusion injury (CIRI) in

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Yoshida, Go J. "The Harmonious Interplay of Amino Acid and Monocarboxylate Transporters Induces the Robustness of Cancer Cells." Metabolites 11, no. 1 (2021): 27. http://dx.doi.org/10.3390/metabo11010027.

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There is a growing body of evidence that metabolic reprogramming contributes to the acquisition and maintenance of robustness associated with malignancy. The fine regulation of expression levels of amino acid and monocarboxylate transporters enables cancer cells to exhibit the metabolic reprogramming that is responsible for therapeutic resistance. Amino acid transporters characterized by xCT (SLC7A11), ASCT2 (SLC1A5), and LAT1 (SLC7A5) function in the uptake and export of amino acids such as cystine and glutamine, thereby regulating glutathione synthesis, autophagy, and glutaminolysis. CD44 va

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Dhaval, V. Patel Mukesh Nandave Prashant S. Kharkar. "PHARMACOPHORE MODELLING FOR THE DISCOVERY OF SYSTEM XC- ANTIPORTER INHIBITORS." August 31, 2017. https://doi.org/10.5281/zenodo.2526801.

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Cancer is one of the major disorders with increasing rates of morbidity and mortality. Recent drug discovery of anti cancer drug has identified several molecular targets and tried to achieve a goal of therapeutic effecative and safe molecule. Amongst these, system xc- antiporter is a novel promising target to control cancer progression. This antiporter is found to be over expressed in majority of cancer cells and functions by transporting amino acids, cystine and glutamate, in opposite directions. System xc- antiporter uptakes one molecule of cystine with the release of one molecule of glutama

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Martin, Abraham, Villoldo Nuria Vazquez, Vallejo Vanessa Gomez, et al. "In vivo imaging of system xc as a novel approach to monitor multiple sclerosis." December 10, 2015. https://doi.org/10.1007/s00259-015-3275-3.

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Glutamate excitotoxicity contributes to oligodendroglial and axonal damage in multiple sclerosis pathology. Extracellular glutamate concentration in the brain is controlled by cystine/glutamate antiporter (system xc), a membrane antiporter that imports cystine and releases glutamate. Despite this, the system xc<sup> </sup> activity and its connection to the inflammatory reaction in multiple sclerosis (MS) is largely unknown.

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Dhaval, Patel Mukesh Nandave and Prashant S. Kharkar*. "PREDICTIVE MODELS FOR SYSTEM XC - ANTIPORTER INHIBITION BASED ON STRUCTURALLY DIVERSE MOLECULES." Indo Am. J. P. Sci, 2017 04, no. 05 (2017). https://doi.org/10.5281/zenodo.582322.

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The morbidity and mortality throughout the world is increasing day by day due to cancer. Several molecular targets have been identified and being targeted for treatment of cancer cells. System xc - , an amino acid antiporter, is one such potential target. With the uptake of one molecule of cystine and release of one molecule glutamate, over expressed system xc -manipulates the redox status within cancer cells and protects them. Simultaneously, released glutamate helps in growth and metastasis of cancer cells. Few researches have synthesized and screened structurally diverse molecules against s

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de Baat, Axel, Daniel T. Meier, Leila Rachid, Adriano Fontana, Marianne Böni-Schnetzler, and Marc Y. Donath. "Cystine/glutamate antiporter System xc- deficiency impairs insulin secretion in mice." Diabetologia, August 31, 2023. http://dx.doi.org/10.1007/s00125-023-05993-6.

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Abstract Aims/hypothesis Glutamate-induced cytotoxicity (excitotoxicity) has been detected in pancreatic beta cells. The cystine/glutamate antiporter System xc- exports glutamate to the extracellular space and is therefore implicated as driving excitotoxicity. As of yet, it has not been investigated whether System xc- contributes to pancreatic islet function. Methods This study describes the implications of deficiency of System xc- on glucose metabolism in both constitutive and myeloid cell-specific knockout mice using metabolic tests and diet-induced obesity. Pancreatic islets were isolated a

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