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ferroptosis

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https://www.readbyqxmd.com/read/29144989/cysteine-dioxygenase-1-mediates-erastin-induced-ferroptosis-in-human-gastric-cancer-cells
#1
Shihui Hao, Jiang Yu, Wanming He, Qiong Huang, Yang Zhao, Bishan Liang, Shuyi Zhang, Zhaowei Wen, Shumin Dong, Jinjun Rao, Wangjun Liao, Min Shi
BACKGROUND: Ferroptosis is a recently discovered form of iron-dependent nonapoptotic cell death. It is characterized by loss of the activity of the lipid repair enzyme, glutathione peroxidase 4 (GPX4), and accumulation of lethal reactive lipid oxygen species. However, we still know relatively little about ferroptosis and its molecular mechanism in gastric cancer (GC) cells. Here, we demonstrate that erastin, a classic inducer of ferroptosis, induces this form of cell death in GC cells and that cysteine dioxygenase 1 (CDO1) plays an important role in this process...
November 13, 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29134661/regulation-of-tmem16a-ano1-and-tmem16f-ano6-ion-currents-and-phospholipid-scrambling-by-ca-2-and-plasma-membrane-lipid
#2
Rainer Schreiber, Jiraporn Ousingsawat, Podchanart Wanitchakool, Lalida Sirianant, Roberta Benedetto, Karina Reiss, Karl Kunzelmann
TMEM16/anoctamin proteins form Ca(2+) activated ion channels or phospholipid scramblases. We found that both TMEM16A/ANO1 and TMEM16F/ANO6 produced Cl(-) currents when activated by intracellular Ca(2+) , but only TMEM16F was able to expose phosphatidylserine to the outer leaflet of the plasma membrane. Mutations within TMEM16F or TMEM16A/F chimeras similarly changed Cl(-) currents and phospholipid scrambling, suggesting the same intramolecular pathway for Cl(-) and phospholipids. When overexpressed, TMEM16A and TMEM16F produced spontaneous Cl(-) currents at 37°C even at resting intracellular Ca(2+) levels, which was abolished by inhibition of phospholipase A2 (PLA2 )...
November 14, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/29134467/diterpenoid-natural-compound-c4-crassin-exerts-cytostatic-effects-on-triple-negative-breast-cancer-cells-via-a-pathway-involving-reactive-oxygen-species
#3
Cathy E Richards, Sri H Vellanki, Yvonne E Smith, Ann M Hopkins
PURPOSE: Triple-negative breast cancers (TNBC) lack expression of three common cell surface receptors, i.e., estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor-2 (HER2). Accordingly, TNBCs are associated with fewer treatment options and a relatively poor prognosis. Having screened a National Cancer Institute natural compound library, the purpose of this study was to investigate the bioactivity of compound C4 (Crassin) in TNBC cells. METHODS: Cell viability assays were performed in two TNBC cell lines, MDA-MB-231 and 4T1, following C4 treatment in the presence or absence of the antioxidant N-acetyl-L-cysteine (NAC)...
November 13, 2017: Cellular Oncology (Dordrecht)
https://www.readbyqxmd.com/read/29127238/protective-effects-of-the-mechanistic-target-of-rapamycin-against-excess-iron-and-ferroptosis-in-cardiomyocytes
#4
Yuichi Baba, Jason K Higa, Briana K Shimada, Kate M Horiuchi, Tomohiro Suhara, Motoi Kobayashi, Jonathan D Woo, Hiroko Aoyagi, Karra S Marh, Hiroaki Kitaoka, Takashi Matsui
Clinical studies suggest that myocardial iron is a risk factor for left ventricular remodeling in patients after myocardial infarction (MI). Ferroptosis was recently reported as a mechanism of iron-dependent non-apoptotic cell death. However, ferroptosis in the heart is not well understood. The mechanistic target of rapamycin (mTOR) protects the heart against pathological stimuli such as ischemia. To define the role of cardiac mTOR on cell survival in iron-mediated cell death, we examined cardiomyocyte (CM) cell viability under excess iron and ferroptosis conditions...
November 10, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29127085/gpx4-inhibition-selectively-targets-drug-tolerant-persister-cells
#5
(no author information available yet)
Targeting GPX4 induces selective cell death of drug-tolerant persister tumor cells by ferroptosis.
November 10, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/29126071/%C3%AE-lipoic-acid-improves-abnormal-behavior-by-mitigation-of-oxidative-stress-inflammation-ferroptosis-and-tauopathy-in-p301s-tau-transgenic-mice
#6
Yan-Hui Zhang, Da-Wei Wang, Shuang-Feng Xu, Shuai Zhang, Yong-Gang Fan, Ying-Ying Yang, Shi-Qi Guo, Shan Wang, Tian Guo, Zhan-You Wang, Chuang Guo
Alzheimer's disease (AD) is the most common neurodegenerative disease and is characterized by neurofibrillary tangles (NFTs) composed of Tau protein. α-Lipoic acid (LA) has been found to stabilize the cognitive function of AD patients, and animal study findings have confirmed its anti-amyloidogenic properties. However, the underlying mechanisms remain unclear, especially with respect to the ability of LA to control Tau pathology and neuronal damage. Here, we found that LA supplementation effectively inhibited the hyperphosphorylation of Tau at several AD-related sites, accompanied by reduced cognitive decline in P301S Tau transgenic mice...
November 7, 2017: Redox Biology
https://www.readbyqxmd.com/read/29081404/socs1-regulates-senescence-and-ferroptosis-by-modulating-the-expression-of-p53-target-genes
#7
Emmanuelle Saint-Germain, Lian Mignacca, Mathieu Vernier, Diwakar Bobbala, Subburaj Ilangumaran, Gerardo Ferbeyre
The mechanism by which p53 suppresses tumorigenesis remains poorly understood. In the context of aberrant activation of the JAK/STAT5 pathway, SOCS1 is required for p53 activation and the regulation of cellular senescence. In order to identify p53 target genes acting during the senescence response to oncogenic STAT5A, we characterized the transcriptome of STAT5A-expressing cells after SOCS1 inhibition. We identified a set of SOCS1-dependent p53 target genes that include several secreted proteins and genes regulating oxidative metabolism and ferroptosis...
October 28, 2017: Aging
https://www.readbyqxmd.com/read/29079265/the-viability-of-primary-hepatocytes-is-maintained-under-a-low-cysteine-glutathione-redox-state-with-a-marked-elevation-in-ophthalmic-acid-production
#8
Jaeyong Lee, Eun Sil Kang, Sho Kobayashi, Takujiro Homma, Hideyo Sato, Han Geuk Seo, Junichi Fujii
Extracellular cystine, the oxidized form of cysteine (Cys), is taken up by cells via the cystine transporter xCT. xCT is not expressed in the liver but is induced in primary hepatocytes under conventional cultured conditions. However, compared to wild-type hepatocytes those from the xCT-knockout mouse showed no evidence of an abnormality and the levels of both Cys and glutathione (GSH) remained unchanged. The levels of ophthalmic acid (OPT), which is produced as an alternative compound by the GSH-synthesizing pathway, became increased during the culturing of hepatocytes...
October 26, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/29055715/live-or-let-die-neuroprotective-and-anti-cancer-effects-of-nutraceutical-antioxidants
#9
REVIEW
Xiao-Yuan Mao, Ming-Zhu Jin, Jin-Fei Chen, Qin Li, Hong-Hao Zhou, Wei-Lin Jin
Diet sources are closely involved in the pathogenesis of diverse neuropsychiatric disorders and cancers, in addition to inherited factors. Currently, natural products or nutraceuticals (commonly called medical foods) are increasingly employed for adjunctive therapy of these patients. However, the potential molecular mechanisms of the nutrient efficacy remain elusive. In this review, we summarized the neuroprotective and anti-cancer mechanisms of nutraceuticals. It was concluded that the nutraceuticals exerted neuroprotection and suppressed tumor growth possibly through the differential modulations of redox homeostasis...
October 18, 2017: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/29053969/pebp1-wardens-ferroptosis-by-enabling-lipoxygenase-generation-of-lipid-death-signals
#10
Sally E Wenzel, Yulia Y Tyurina, Jinming Zhao, Claudette M St Croix, Haider H Dar, Gaowei Mao, Vladimir A Tyurin, Tamil S Anthonymuthu, Alexandr A Kapralov, Andrew A Amoscato, Karolina Mikulska-Ruminska, Indira H Shrivastava, Elizabeth M Kenny, Qin Yang, Joel C Rosenbaum, Louis J Sparvero, David R Emlet, Xiaoyan Wen, Yoshinori Minami, Feng Qu, Simon C Watkins, Theodore R Holman, Andrew P VanDemark, John A Kellum, Ivet Bahar, Hülya Bayır, Valerian E Kagan
Ferroptosis is a form of programmed cell death that is pathogenic to several acute and chronic diseases and executed via oxygenation of polyunsaturated phosphatidylethanolamines (PE) by 15-lipoxygenases (15-LO) that normally use free polyunsaturated fatty acids as substrates. Mechanisms of the altered 15-LO substrate specificity are enigmatic. We sought a common ferroptosis regulator for 15LO. We discovered that PEBP1, a scaffold protein inhibitor of protein kinase cascades, complexes with two 15LO isoforms, 15LO1 and 15LO2, and changes their substrate competence to generate hydroperoxy-PE...
October 19, 2017: Cell
https://www.readbyqxmd.com/read/29053966/transforming-lipoxygenases-pe-specific-enzymes-in-disguise
#11
Ling F Ye, Brent R Stockwell
In this issue of Cell, Wenzel et al. solve a long-standing mystery regarding how damage to cell membranes occurs during ferroptosis, an iron-dependent form of regulated cell death. They found that lipoxygenases are like Transformer toys, being converted from one enzyme type to another in the presence of the protein PEBP1.
October 19, 2017: Cell
https://www.readbyqxmd.com/read/29052145/cell-death-pathways-a-novel-therapeutic-approach-for-neuroscientists
#12
REVIEW
G Morris, A J Walker, M Berk, M Maes, B K Puri
In the first part, the following mechanisms involved in different forms of cell death are considered, with a view to identifying potential therapeutic targets: tumour necrosis factor receptors (TNFRs) and their engagement by tumour necrosis factor-alpha (TNF-α); poly [ADP-ribose] polymerase (PARP)-1 cleavage; the apoptosis signalling kinase (ASK)-c-Jun N-terminal kinase (JNK) axis; lysosomal permeability; activation of programmed necrotic cell death; oxidative stress, caspase-3 inhibition and parthanatos; activation of inflammasomes by reactive oxygen species and the development of pyroptosis; oxidative stress, calcium dyshomeostasis and iron in the development of lysosomal-mediated necrosis and lysosomal membrane permeability; and oxidative stress, lipid peroxidation, iron dyshomeostasis and ferroptosis...
October 19, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29038744/autophagy-and-ferroptosis-what-s-the-connection
#13
Rui Kang, Daolin Tang
PURPOSE OF REVIEW: Autophagy is a conserved intracellular degradation system and plays a dual role in cell death, depending on context and phase. Ferroptosis is a new form of regulated cell death that mainly depends on iron accumulation and lipid peroxidation. In this review, we summarize the processes of autophagy and ferroptosis and discuss their crosstalk mechanisms at the molecular level. RECENT FINDINGS: The original study shows that ferroptosis is morphologically, biochemically, and genetically distinct from autophagy and other types of cell death...
June 2017: Current Pathobiology Reports
https://www.readbyqxmd.com/read/29037212/chromatin-remodeling-factor-lymphoid-specific-helicase-inhibits-ferroptosis-through-lipid-metabolic-genes-in-lung-cancer-progression
#14
Yiqun Jiang, Yuchen He, Shuang Liu, Yongguang Tao
No abstract text is available yet for this article.
October 16, 2017: Chinese Journal of Cancer
https://www.readbyqxmd.com/read/28985560/ferroptosis-a-regulated-cell-death-nexus-linking-metabolism-redox-biology-and-disease
#15
REVIEW
Brent R Stockwell, José Pedro Friedmann Angeli, Hülya Bayir, Ashley I Bush, Marcus Conrad, Scott J Dixon, Simone Fulda, Sergio Gascón, Stavroula K Hatzios, Valerian E Kagan, Kay Noel, Xuejun Jiang, Andreas Linkermann, Maureen E Murphy, Michael Overholtzer, Atsushi Oyagi, Gabriela C Pagnussat, Jason Park, Qitao Ran, Craig S Rosenfeld, Konstantin Salnikow, Daolin Tang, Frank M Torti, Suzy V Torti, Shinya Toyokuni, K A Woerpel, Donna D Zhang
Ferroptosis is a form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels. Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused by the incorporation of polyunsaturated fatty acids into cellular membranes, and cells have developed complex systems that exploit and defend against this vulnerability in different contexts. The sensitivity to ferroptosis is tightly linked to numerous biological processes, including amino acid, iron, and polyunsaturated fatty acid metabolism, and the biosynthesis of glutathione, phospholipids, NADPH, and coenzyme Q10...
October 5, 2017: Cell
https://www.readbyqxmd.com/read/28985506/nrf2-is-a-major-target-of-arf-in-p53-independent-tumor-suppression
#16
Delin Chen, Omid Tavana, Bo Chu, Luke Erber, Yue Chen, Richard Baer, Wei Gu
Although ARF can suppress tumor growth by activating p53 function, the mechanisms by which it suppresses tumor growth independently of p53 are not well understood. Here, we identified ARF as a key regulator of nuclear factor E2-related factor 2 (NRF2) through complex purification. ARF inhibits the ability of NRF2 to transcriptionally activate its target genes, including SLC7A11, a component of the cystine/glutamate antiporter that regulates reactive oxygen species (ROS)-induced ferroptosis. As a consequence, ARF expression sensitizes cells to ferroptosis in a p53-independent manner while ARF depletion induces NRF2 activation and promotes cancer cell survival in response to oxidative stress...
October 5, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28984871/how-do-we-fit-ferroptosis-in-the-family-of-regulated-cell-death
#17
REVIEW
Howard O Fearnhead, Peter Vandenabeele, Tom Vanden Berghe
In the last few years many new cell death modalities have been described. To classify different types of cell death, the term 'regulated cell death' was introduced to discriminate it from 'accidental cell death'. Regulated cell death involves the activation of genetically encoded molecular machinery that couples the presence of some signal to cell death. These forms of cell death, like apoptosis, necroptosis and pyroptosis have important physiological roles in development, tissue repair, and immunity. Accidental cell death occurs in response to physical or chemical insults and occurs independently of molecular signalling pathways...
December 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28975372/t-buooh-induces-ferroptosis-in-human-and-murine-cell-lines
#18
Christine Wenz, Dagmar Faust, Berenike Linz, Christian Turmann, Teodora Nikolova, John Bertin, Peter Gough, Peter Wipf, Anna Sophia Schröder, Stefan Krautwald, Cornelia Dietrich
Reactive oxygen species (ROS)-induced apoptosis has been extensively studied. Increasing evidence suggests that ROS, for instance, induced by hydrogen peroxide (H2O2), might also trigger regulated necrotic cell death pathways. Almost nothing is known about the cell death pathways triggered by tertiary-butyl hydroperoxide (t-BuOOH), a widely used inducer of oxidative stress. The lipid peroxidation products induced by t-BuOOH are involved in the pathophysiology of many diseases, such as cancer, cardiovascular diseases, or diabetes...
October 3, 2017: Archives of Toxicology
https://www.readbyqxmd.com/read/28972104/the-%C3%AE-6%C3%AE-4-integrin-promotes-resistance-to-ferroptosis
#19
Caitlin W Brown, John J Amante, Hira Lal Goel, Arthur M Mercurio
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...
September 28, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28937680/salinomycin-kills-cancer-stem-cells-by-sequestering-iron-in-lysosomes
#20
Trang Thi Mai, Ahmed Hamaï, Antje Hienzsch, Tatiana Cañeque, Sebastian Müller, Julien Wicinski, Olivier Cabaud, Christine Leroy, Amandine David, Verónica Acevedo, Akihide Ryo, Christophe Ginestier, Daniel Birnbaum, Emmanuelle Charafe-Jauffret, Patrice Codogno, Maryam Mehrpour, Raphaël Rodriguez
Cancer stem cells (CSCs) represent a subset of cells within tumours that exhibit self-renewal properties and the capacity to seed tumours. CSCs are typically refractory to conventional treatments and have been associated to metastasis and relapse. Salinomycin operates as a selective agent against CSCs through mechanisms that remain elusive. Here, we provide evidence that a synthetic derivative of salinomycin, which we named ironomycin (AM5), exhibits a more potent and selective activity against breast CSCs in vitro and in vivo, by accumulating and sequestering iron in lysosomes...
October 2017: Nature Chemistry
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