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ferroptosis

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https://www.readbyqxmd.com/read/29356212/emerging-strategies-of-cancer-therapy-based-on-ferroptosis
#1
REVIEW
Zheyu Shen, Jibin Song, Bryant C Yung, Zijian Zhou, Aiguo Wu, Xiaoyuan Chen
Ferroptosis, a new form of regulated cell death that is iron- and reactive oxygen species dependent, has attracted much attention in the research communities of biochemistry, oncology, and especially material sciences. Since the first demonstration in 2012, a series of strategies have been developed to induce ferroptosis of cancer cells, including the use of nanomaterials, clinical drugs, experimental compounds, and genes. A plethora of research work has outlined the blueprint of ferroptosis as a new option for cancer therapy...
January 22, 2018: Advanced Materials
https://www.readbyqxmd.com/read/29348676/mir-137-regulates-ferroptosis-by-targeting-glutamine-transporter-slc1a5-in-melanoma
#2
Meiying Luo, Longfei Wu, Kexin Zhang, Hong Wang, Tian Zhang, Lucas Gutierrez, Douglas O'Connell, Peng Zhang, Yu Li, Tongtong Gao, Wenyan Ren, Yongfei Yang
Ferroptosis is a regulated form of cell death driven by small molecules or conditions that induce lipid-based reactive oxygen species (ROS) accumulation. This form of iron-dependent cell death is morphologically and genetically distinct from apoptosis, necroptosis, and autophagy. miRNAs are known to play crucial roles in diverse fundamental biological processes. However, to date no study has reported miRNA-mediated regulation of ferroptosis. Here we show that miR-137 negatively regulates ferroptosis by directly targeting glutamine transporter SLC1A5 in melanoma cells...
January 18, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29346757/p53-suppresses-metabolic-stress-induced-ferroptosis-in-cancer-cells
#3
Amy Tarangelo, Leslie Magtanong, Kathryn T Bieging-Rolett, Yang Li, Jiangbin Ye, Laura D Attardi, Scott J Dixon
How cancer cells respond to nutrient deprivation remains poorly understood. In certain cancer cells, deprivation of cystine induces a non-apoptotic, iron-dependent form of cell death termed ferroptosis. Recent evidence suggests that ferroptosis sensitivity may be modulated by the stress-responsive transcription factor and canonical tumor suppressor protein p53. Using CRISPR/Cas9 genome editing, small-molecule probes, and high-resolution, time-lapse imaging, we find that stabilization of wild-type p53 delays the onset of ferroptosis in response to cystine deprivation...
January 16, 2018: Cell Reports
https://www.readbyqxmd.com/read/29343855/the-ferroptosis-inducer-erastin-irreversibly-inhibits-system-xc-and-synergizes-with-cisplatin-to-increase-cisplatin-s-cytotoxicity-in-cancer-cells
#4
Mami Sato, Ryosuke Kusumi, Shinji Hamashima, Sho Kobayashi, Satoru Sasaki, Yuhei Komiyama, Takuji Izumikawa, Marcus Conrad, Shiro Bannai, Hideyo Sato
System xc- was recently described as the most upstream node in a novel form of regulated necrotic cell death, called ferroptosis. In this context, the small molecule erastin was reported to target and inhibit system xc-, leading to cysteine starvation, glutathione depletion and consequently ferroptotic cell death. Although the inhibitory effect of erastin towards system xc- is well-documented, nothing is known about its mechanism of action. Therefore, we sought to interrogate in more detail the underlying mechanism of erastin's pro-ferroptotic effects...
January 17, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29331741/extracellular-acidification-induces-ros-and-mptp-mediated-death-in-hek293-cells
#5
José Teixeira, Farhan Basit, Herman G Swarts, Marleen Forkink, Paulo J Oliveira, Peter H G M Willems, Werner J H Koopman
The extracellular pH (pHe) is a key determinant of the cellular (micro)environment and needs to be maintained within strict boundaries to allow normal cell function. Here we used HEK293 cells to study the effects of pHe acidification (24h), induced by mitochondrial inhibitors (rotenone, antimycin A) and/or extracellular HCl addition. Lowering pHe from 7.2 to 5.8 reduced cell viability by 70% and was paralleled by a decrease in cytosolic pH (pHc), hyperpolarization of the mitochondrial membrane potential (Δψ), increased levels of hydroethidine-oxidizing ROS and stimulation of protein carbonylation...
December 30, 2017: Redox Biology
https://www.readbyqxmd.com/read/29330409/induction-of-ferroptosis-and-mitochondrial-dysfunction-by-oxidative-stress-in-pc12-cells
#6
Chuanhong Wu, Wenwen Zhao, Jie Yu, Shaojing Li, Ligen Lin, Xiuping Chen
Neurodegenerative diseases (NDD) are typically associated with neuron loss in nervous system areas. Interventions with related death mechanisms may ameliorate NDD progression. Oxidative stress plays an important role in NDD cell death routines. However, tert-butylhydroperoxide (t-BHP), a widely used oxidative stress stimulus, induces neural cell death through a mechanism that remains elusive. In our study, the ferroptosis marker events occurred after co-treatment with 100 μM t-BHP for 1 h, all of which were reversed in the presence of the ferroptosis inhibitor ferrostatin-1 (Fer-1) and the iron chelator deferoxamine, implying the occurrence of ferroptosis...
January 12, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29322476/negative-regulators-of-cell-death-pathways-in-cancer-perspective-on-biomarkers-and-targeted-therapies
#7
REVIEW
Ali Razaghi, Kirsten Heimann, Patrick M Schaeffer, Spencer B Gibson
Cancer is a primary cause of human fatality and conventional cancer therapies, e.g., chemotherapy, are often associated with adverse side-effects, tumor drug-resistance, and recurrence. Molecularly targeted therapy, composed of small-molecule inhibitors and immunotherapy (e.g., monoclonal antibody and cancer vaccines), is a less harmful alternative being more effective against cancer cells whilst preserving healthy tissues. Drug-resistance, however, caused by negative regulation of cell death signaling pathways, is still a challenge...
January 10, 2018: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/29306548/disrupting-the-warburg-effect-re-routes-cancer-cells-to-oxphos-offering-a-vulnerability-point-via-ferroptosis-induced-cell-death
#8
REVIEW
Maša Ždralević, Milica Vučetić, Boutaina Daher, Ibtissam Marchiq, Scott K Parks, Jacques Pouysségur
The evolution of life from extreme hypoxic environments to an oxygen-rich atmosphere has progressively selected for successful metabolic, enzymatic and bioenergetic networks through which a myriad of organisms survive the most extreme environmental conditions. From the two lethal environments anoxia/high O2, cells have developed survival strategies through expression of the transcriptional factors ATF4, HIF1 and NRF2. Cancer cells largely exploit these factors to thrive and resist therapies. In this review, we report and discuss the potential therapeutic benefit of disrupting the major Myc/Hypoxia-induced metabolic pathway, also known as fermentative glycolysis or "Warburg effect", in aggressive cancer cell lines...
December 28, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29290465/selenium-utilization-by-gpx4-is-required-to-prevent-hydroperoxide-induced-ferroptosis
#9
Irina Ingold, Carsten Berndt, Sabine Schmitt, Sebastian Doll, Gereon Poschmann, Katalin Buday, Antonella Roveri, Xiaoxiao Peng, Florencio Porto Freitas, Tobias Seibt, Lisa Mehr, Michaela Aichler, Axel Walch, Daniel Lamp, Martin Jastroch, Sayuri Miyamoto, Wolfgang Wurst, Fulvio Ursini, Elias S J Arnér, Noelia Fradejas-Villar, Ulrich Schweizer, Hans Zischka, José Pedro Friedmann Angeli, Marcus Conrad
Selenoproteins are rare proteins among all kingdoms of life containing the 21st amino acid, selenocysteine. Selenocysteine resembles cysteine, differing only by the substitution of selenium for sulfur. Yet the actual advantage of selenolate- versus thiolate-based catalysis has remained enigmatic, as most of the known selenoproteins also exist as cysteine-containing homologs. Here, we demonstrate that selenolate-based catalysis of the essential mammalian selenoprotein GPX4 is unexpectedly dispensable for normal embryogenesis...
December 16, 2017: Cell
https://www.readbyqxmd.com/read/29289598/why-should-neuroscientists-worry-about-iron-the-emerging-role-of-ferroptosis-in-the-pathophysiology-of-neuroprogressive-diseases
#10
REVIEW
Gerwyn Morris, Michael Berk, André F Carvalho, Michael Maes, Adam J Walker, Basant K Puri
Ferroptosis is a unique form of programmed death, characterised by cytosolic accumulation of iron, lipid hydroperoxides and their metabolites, and effected by the fatal peroxidation of polyunsaturated fatty acids in the plasma membrane. It is a major driver of cell death in neurodegenerative neurological diseases. Moreover, cascades underpinning ferroptosis could be active drivers of neuropathology in major psychiatric disorders. Oxidative and nitrosative stress can adversely affect mechanisms and proteins governing cellular iron homeostasis, such as the iron regulatory protein/iron response element system, and can ultimately be a source of abnormally high levels of iron and a source of lethal levels of lipid membrane peroxidation...
December 28, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/29289511/opening-of-voltage-dependent-anion-channels-promotes-reactive-oxygen-species-generation-mitochondrial-dysfunction-and-cell-death-in-cancer-cells
#11
David N DeHart, Diana Fang, Kareem Heslop, Li Li, John J Lemasters, Eduardo N Maldonado
Enhancement of aerobic glycolysis and suppression of mitochondrial metabolism characterize the pro-proliferative Warburg phenotype of cancer cells. High free tubulin in cancer cells closes voltage dependent anion channels (VDAC) to decrease mitochondrial membrane potential (ΔΨ), an effect antagonized by erastin, the canonical promotor of ferroptosis. Previously, we identified six compounds (X1-X6) that also block tubulin-dependent mitochondrial depolarization. Here, we hypothesized that VDAC opening after erastin and X1-X6 increases mitochondrial metabolism and reactive oxygen species (ROS) formation, leading to ROS-dependent mitochondrial dysfunction, bioenergetic failure and cell death...
December 28, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29282302/acid-sphingomyelinase-promotes-mitochondrial-dysfunction-due-to-glutamate-induced-regulated-necrosis
#12
Sergei A Novgorodov, Joshua R Voltin, Monika A Gooz, Li Li, John J Lemasters, Tatyana I Gudz
Inhibiting the glutamate/cystine antiporter system xc-, a key antioxidant defense machinery in the CNS, could trigger a novel form of regulated necrotic cell death, ferroptosis. The underlying mechanisms of system xc--dependent cell demise were elucidated using primary oligodendrocytes (OLs) treated with glutamate to block system xc- function. Pharmacological analysis revealed ferroptosis as a major contributing factor to glutamate-initiated OL death. Sphingolipid profile showed elevations of ceramide species and sphingosine that were preventable by inhibiting of an acid sphingomyelinase (ASM) activity...
December 27, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/29274359/ho-1-mediates-bay-11-7085-induced-ferroptosis
#13
Ling-Chu Chang, Shih-Kai Chiang, Shuen-Ei Chen, Yung-Luen Yu, Ruey-Hwang Chou, Wei-Chao Chang
Ferroptosis is a form of oxidative cell death and has become a chemotherapeutic target for cancer treatment. BAY 11-7085 (BAY), which is a well-known IκBα inhibitor, suppressed viability in cancer cells via induction of ferroptotic death in a NF-κB-independent manner. Reactive oxygen species scavenging, relief of lipid peroxidation, replenishment of glutathione and thiol-containing agents, as well as iron chelation, rescued BAY-induced cell death. BAY upregulated a variety of Nrf2 target genes related to redox regulation, particularly heme oxygenase-1 (HO-1)...
December 20, 2017: Cancer Letters
https://www.readbyqxmd.com/read/29248440/jtc801-induces-ph-dependent-death-specifically-in-cancer-cells-and-slows-growth-of-tumors-in-mice
#14
Xinxin Song, Shan Zhu, Yangchun Xie, Jiao Liu, Lingyi Sun, Dexing Zeng, Pengcheng Wang, Xiaochao Ma, Guido Kroemer, David L Bartlett, Timothy R Billiar, Michael Lotze, Herbert Zeh, Rui Kang, Daolin Tang
BACKGROUND & AIMS: Maintenance of acid-base homeostasis is required for normal physiology, metabolism, and development. It is not clear how cell death is activated in response to changes in pH. We performed a screen to identify agents that induce cell death in a pH-dependent manner (we call this alkaliptosis) in pancreatic ductal adenocarcinoma cancer (PDAC) cells and tested their effects in mice. METHODS: We screened a library of 254 compounds that interact with G protein-coupled receptors (GPCRs) to identify those with cytotoxic activity against a human PDAC cell line (PANC1)...
December 14, 2017: Gastroenterology
https://www.readbyqxmd.com/read/29235250/discovery-and-mechanistic-elucidation-of-a-class-of-pdi-inhibitors-for-the-treatment-of-glioblastoma
#15
Anahita Kyani, Shuzo Tamura, Suhui Yang, Andrea Shergalis, Soma Somanta, Yuting Kuang, Mats Ljungman, Nouri Neamati
Protein disulfide isomerase (PDI) is overexpressed in glioblastoma, the most aggressive form of brain cancer, and folds nascent proteins responsible for the progression and spread of the disease. Herein, we describe a novel, nanomolar PDI inhibitor, pyrimidotriazinedione 35G8, that is toxic in a panel of human glioblastoma cell lines. We performed a medium throughput 20,000-compound screen of a diverse subset of 1,000,000 compounds to identify cytotoxic small molecules. Cytotoxic compounds were screened for PDI inhibition, and, from the screen, 35G8 emerged as the most cytotoxic inhibitor of PDI...
December 12, 2017: ChemMedChem
https://www.readbyqxmd.com/read/29234486/jnk-signaling-a-multiplexing-hub-in-programmed-cell-death
#16
REVIEW
Danny N Dhanasekaran, E Premkumar Reddy
Jun N-terminal kinases or JNKs have been shown to be involved in a wide array of signaling events underlying tumorigenesis and tumor progression. Through its interaction with a diverse set of signaling proteins and adaptors, JNKs regulate cell proliferation, invasive migration, therapy resistance, and programmed cell death. JNKs have been shown to play a role in apoptotic as well as non-apoptotic programmed cell death mechanisms including those of necroptosis, ferroptosis, pyroptosis, and autophagy. Most of the tumorigenic regulatory functions of JNKs can be related to their ability to module cell death via these programmed cell death mechanisms...
September 2017: Genes & Cancer
https://www.readbyqxmd.com/read/29223642/fighting-resilient-cancers-with-iron
#17
Jonathan J Chen, Lorenzo Galluzzi
Tumor progression and resistance to treatment are often accompanied by the polarization of malignant cells towards a mesenchymal or poorly differentiated state. Such a transition generates an accrued vulnerability to the induction of ferroptosis, potentially paving the way to novel therapeutic strategies for targeting residual disease in patients with cancer.
December 6, 2017: Trends in Cell Biology
https://www.readbyqxmd.com/read/29222191/nfs1-expression-protects-lung-tumor-cells-from-ferroptosis
#18
(no author information available yet)
NFS1 activity is essential for maintenance of iron-sulfur cluster biosynthesis in response to oxidative stress.
December 8, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/29212794/ferroptosis-beating-on-death-s-door
#19
Rimpy Dhingra, Amir Ravandi, Lorrie A Kirshenbaum
One of the most fascinating concepts to impact contemporary biology to date is the idea that cell death is a highly regulated and programmed event. Cardiac cells can die by apoptosis or necrosis and in some instances by autophagy. Ferroptosis, is a new form of regulated cell death that is gaining considerable attention, that links de-regulated iron metabolism with peroxidative lipid injury. In this report, we highlight a recent study by Baba et al that describes ferroptosis as regulated form of cell death in the heart...
December 6, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29212036/%C3%AE-np63-inhibits-oxidative-stress-induced-cell-death-including-ferroptosis-and-cooperates-with-the-bcl-2-family-to-promote-clonogenic-survival
#20
Gary X Wang, Ho-Chou Tu, Yiyu Dong, Anders Jacobsen Skanderup, Yufeng Wang, Shugaku Takeda, Yogesh Tengarai Ganesan, Song Han, Han Liu, James J Hsieh, Emily H Cheng
The BCL-2 family proteins are central regulators of apoptosis. However, cells deficient for BAX and BAK or overexpressing BCL-2 still succumb to oxidative stress upon DNA damage or matrix detachment. Here, we show that ΔNp63α overexpression protects cells from oxidative stress induced by oxidants, DNA damage, anoikis, or ferroptosis-inducing agents. Conversely, ΔNp63α deficiency increases oxidative stress. Mechanistically, ΔNp63α orchestrates redox homeostasis through transcriptional control of glutathione biogenesis, utilization, and regeneration...
December 5, 2017: Cell Reports
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