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https://www.readbyqxmd.com/read/28319068/iron-addiction-a-novel-therapeutic-target-in-ovarian-cancer
#1
D Basuli, L Tesfay, Z Deng, B Paul, Y Yamamoto, G Ning, W Xian, F McKeon, M Lynch, C P Crum, P Hegde, M Brewer, X Wang, L D Miller, N Dyment, F M Torti, S V Torti
Ovarian cancer is a lethal malignancy that has not seen a major therapeutic advance in over 30 years. We demonstrate that ovarian cancer exhibits a targetable alteration in iron metabolism. Ferroportin (FPN), the iron efflux pump, is decreased, and transferrin receptor (TFR1), the iron importer, is increased in tumor tissue from patients with high grade but not low grade serous ovarian cancer. A similar profile of decreased FPN and increased TFR1 is observed in a genetic model of ovarian cancer tumor-initiating cells (TICs)...
March 20, 2017: Oncogene
https://www.readbyqxmd.com/read/28297659/oncogene-selective-sensitivity-to-synchronous-cell-death-following-modulation-of-the-amino-acid-nutrient-cystine
#2
Ioannis Poursaitidis, Xiaomeng Wang, Thomas Crighton, Christiaan Labuschagne, David Mason, Shira L Cramer, Kendra Triplett, Rajat Roy, Olivier E Pardo, Michael J Seckl, Scott W Rowlinson, Everett Stone, Richard F Lamb
Cancer cells reprogram their metabolism, altering both uptake and utilization of extracellular nutrients. We individually depleted amino acid nutrients from isogenic cells expressing commonly activated oncogenes to identify correspondences between nutrient supply and viability. In HME (human mammary epithelial) cells, deprivation of cystine led to increased cell death in cells expressing an activated epidermal growth factor receptor (EGFR) mutant. Cell death occurred via synchronous ferroptosis, with generation of reactive oxygen species (ROS)...
March 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28276141/iron-and-ferroptosis-a-still-ill-defined-liaison
#3
REVIEW
Sebastian Doll, Marcus Conrad
Ferroptosis is a recently described form of regulated necrotic cell death, which appears to contribute to a number of diseases, such as tissue ischemia/reperfusion injury, acute renal failure, and neurodegeneration. A hallmark of ferroptosis is iron-dependent lipid peroxidation, which can be inhibited by the key ferroptosis regulator glutathione peroxidase 4(Gpx4), radical trapping antioxidants and ferroptosis-specific inhibitors, such as ferrostatins and liproxstatins, as well as iron chelation. Although great strides have been made towards a better understanding of the proximate signals of distinctive lipid peroxides in ferroptosis, still little is known about the mechanistic implication of iron in the ferroptotic process...
March 9, 2017: IUBMB Life
https://www.readbyqxmd.com/read/28254675/from-ancient-herb-to-modern-drug-artemisia-annua-and-artemisinin-for-cancer-therapy
#4
REVIEW
Thomas Efferth
Artemisia annua L. is used throughout Asia and Africa as tea and press juice to treat malaria and related symptomes (fever, chills). Its active ingredient, artemisinin (ARS), has been developed as antimalarial drug and is used worldwide. Interestingly, the bioactivity is not restricted to malaria treatment. We and others found that ARS-type drugs also reveal anticancer in vitro and in vivo. In this review, we give a systematic overview of the literature published over the past two decades until the end of 2016...
February 28, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/28250973/mpp-induces-necrostatin-1-and-ferrostatin-1-sensitive-necrotic-death-of-neuronal-sh-sy5y-cells
#5
Keisuke Ito, Yutaka Eguchi, Yusuke Imagawa, Shuji Akai, Hideki Mochizuki, Yoshihide Tsujimoto
Regulation of cell death is potentially a powerful treatment modality for intractable diseases such as neurodegenerative diseases. Although there have been many reports about the possible involvement of various types of cell death in neurodegenerative diseases, it is still unclear exactly how neurons die in patients with these diseases, thus treatment strategies based on cell death regulation have not been established yet. To obtain some insight into the mechanisms of cell death involved in neurodegenerative diseases, we studied the effect of 1-methyl-4-phenylpyridinium (MPP+) on the human neuroblastoma cell line SH-SY5Y (a widely used model of Parkinson's disease)...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28250197/neuronal-death-after-hemorrhagic-stroke-in-vitro-and-in-vivo-shares-features-of-ferroptosis-and-necroptosis
#6
Marietta Zille, Saravanan S Karuppagounder, Yingxin Chen, Peter J Gough, John Bertin, Joshua Finger, Teresa A Milner, Elizabeth A Jonas, Rajiv R Ratan
BACKGROUND AND PURPOSE: Intracerebral hemorrhage leads to disability or death with few established treatments. Adverse outcomes after intracerebral hemorrhage result from irreversible damage to neurons resulting from primary and secondary injury. Secondary injury has been attributed to hemoglobin and its oxidized product hemin from lysed red blood cells. The aim of this study was to identify the underlying cell death mechanisms attributable to secondary injury by hemoglobin and hemin to broaden treatment options...
March 1, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28246195/ferroptosis-like-cell-death-in-plants
#7
Alexandra A Mushegian
Heat stress induces a form of cell death in plants that is morphologically and biochemically similar to ferroptosis in animal cells.
February 28, 2017: Science Signaling
https://www.readbyqxmd.com/read/28212525/ablation-of-ferroptosis-regulator-glutathione-peroxidase-4-in-forebrain-neurons-promotes-cognitive-impairment-and-neurodegeneration
#8
William Sealy Hambright, Rene Solano Fonseca, Liuji Chen, Ren Na, Qitao Ran
Synaptic loss and neuron death are the underlying cause of neurodegenerative diseases such as Alzheimer's disease (AD); however, the modalities of cell death in those diseases remain unclear. Ferroptosis, a newly identified oxidative cell death mechanism triggered by massive lipid peroxidation, is implicated in the degeneration of neurons populations such as spinal motor neurons and midbrain neurons. Here, we investigated whether neurons in forebrain regions (cerebral cortex and hippocampus) that are severely afflicted in AD patients might be vulnerable to ferroptosis...
February 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28204974/lipid-peroxidation-dependent-cell-death-regulated-by-gpx4-and-ferroptosis
#9
Hirotaka Imai, Masaki Matsuoka, Takeshi Kumagai, Taro Sakamoto, Tomoko Koumura
Glutathione peroxidase 4 (Phospholipid hydroperoxide glutathione peroxidase, PHGPx) can directly reduce phospholipid hydroperoxide. Depletion of GPx4 induces lipid peroxidation-dependent cell death in embryo, testis, brain, liver, heart, and photoreceptor cells of mice. Administration of vitamin E in tissue specific GPx4 KO mice restored tissue damage in testis, liver, and heart. These results indicate that suppression of phospholipid peroxidation is essential for cell survival in normal tissues in mice. Ferroptosis is an iron-dependent non-apoptotic cell death that can elicited by pharmacological inhibiting the cystine/glutamate antiporter, system Xc(-) (type I) or directly binding and loss of activity of GPx4 (Type II) in cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression, but not in normal cells...
February 16, 2017: Current Topics in Microbiology and Immunology
https://www.readbyqxmd.com/read/28203523/glutathione-peroxidase-4-plays-an-important-role-in-oxidative-homeostasis-and-wound-repair-in-corneal-epithelial-cells
#10
Osamu Sakai, Takatoshi Uchida, Hirotaka Imai, Takashi Ueta
Oxidative stress is involved in the pathologies of corneal epithelial cells. However, the importance of specific antioxidant enzymes in corneal epithelial cells is not fully understood. The purpose of this study is to elucidate the role of glutathione peroxidase 4 (GPx4) in corneal epithelial cells. For in vitro experiments, an immortalized human corneal epithelial cell line was used. Cytotoxicity measured through LDH activity, lipid peroxidation immunostained for 4-hydroxynonenal, cell viability, and cell death were compared between cells transfected with either GPx4 siRNA or scrambled control siRNA...
December 2016: FEBS Open Bio
https://www.readbyqxmd.com/read/28195347/characterization-of-ferroptosis-in-murine-models-of-hemochromatosis
#11
Hao Wang, Peng An, Enjun Xie, Qian Wu, Xuexian Fang, Hong Gao, Zhuzhen Zhang, Yuzhu Li, Xudong Wang, Jiaying Zhang, Guoli Li, Lei Yang, Wei Liu, Junxia Min, Fudi Wang
Ferroptosis is a recently identified iron-dependent form of non-apoptotic cell death implicated in brain, kidney, and heart pathology. However, the biological roles of iron and iron metabolism in ferroptosis remain poorly understood. Here, we studied the functional role of iron and iron metabolism in the pathogenesis of ferroptosis. We found that ferric citrate potently induces ferroptosis in murine primary hepatocytes and bone marrow-derived macrophages (BMDMs). Next, we screened for ferroptosis in mice fed a high-iron diet and in mouse models of hereditary hemochromatosis with iron overload...
February 13, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28130223/hspa5-regulates-ferroptotic-cell-death-in-cancer-cells
#12
Shan Zhu, Qiuhong Zhang, Xiaofang Sun, Herbert J Zeh, Michael T Lotze, Rui Kang, Daolin Tang
Ferroptosis is a form of regulated cell death driven by oxidative injury promoting lipid peroxidation, although detailed molecular regulators are largely unknown. Here we show that heat shock 70kDa protein 5 (HSPA5) negatively regulates ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cells. Mechanistically, activating transcription factor 4 (ATF4) resulted in the induction of HSPA5, which in turn bound glutathione peroxidase 4 (GPX4) and protected against GPX4 protein degradation and subsequent lipid peroxidation...
January 27, 2017: Cancer Research
https://www.readbyqxmd.com/read/28108525/back-to-the-roots-of-regulated-necrosis
#13
Vladimir Todorov, Andreas Linkermann
In recent years, our knowledge of how cells die by regulated pathways of necrosis has increased tremendously. In this issue, Distéfano et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201605110) provide yet another milestone in our understanding of regulated necrosis as they identify a ferroptosis-like cell death in Arabidopsis thaliana.
February 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28100685/heat-stress-induces-ferroptosis-like-cell-death-in-plants
#14
Ayelén Mariana Distéfano, María Victoria Martin, Juan Pablo Córdoba, Andrés Martín Bellido, Sebastián D'Ippólito, Silvana Lorena Colman, Débora Soto, Juan Alfredo Roldán, Carlos Guillermo Bartoli, Eduardo Julián Zabaleta, Diego Fernando Fiol, Brent R Stockwell, Scott J Dixon, Gabriela Carolina Pagnussat
In plants, regulated cell death (RCD) plays critical roles during development and is essential for plant-specific responses to abiotic and biotic stresses. Ferroptosis is an iron-dependent, oxidative, nonapoptotic form of cell death recently described in animal cells. In animal cells, this process can be triggered by depletion of glutathione (GSH) and accumulation of lipid reactive oxygen species (ROS). We investigated whether a similar process could be relevant to cell death in plants. Remarkably, heat shock (HS)-induced RCD, but not reproductive or vascular development, was found to involve a ferroptosis-like cell death process...
February 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28088622/reactive-oxygen-species-and-cancer-paradox-to-promote-or-to-suppress
#15
REVIEW
Sehamuddin Galadari, Anees Rahman, Siraj Pallichankandy, Faisal Thayyullathil
Reactive oxygen species (ROS), a group of highly reactive ions and molecules, are increasingly being appreciated as powerful signaling molecules involved in the regulation of a variety of biological processes. Indeed, their role is continuously being delineated in a variety of pathophysiological conditions. For instance, cancer cells are shown to have increased ROS levels in comparison to their normal counterparts. This is partly due to an enhanced metabolism and mitochondrial dysfunction in cancer cells. The escalated ROS generation in cancer cells contributes to the biochemical and molecular changes necessary for the tumor initiation, promotion and progression, as well as, tumor resistance to chemotherapy...
March 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28027643/switching-apoptosis-to-ferroptosis-metal-organic-network-for-high-efficiency-anticancer-therapy
#16
Di-Wei Zheng, Qi Lei, Jing-Yi Zhu, Jin-Xuan Fan, Chu-Xin Li, Cao Li, Zushun Xu, Si-Xue Cheng, Xian-Zheng Zhang
Discovering advanced materials for regulating cell death is of great importance in the development of anticancer therapy. Herein, by harnessing the recently discovered oxidative stress regulation ability of p53 and the Fenton reaction inducing capability of metal-organic network (MON), MON encapsulated with p53 plasmid (MON-p53) was designed to eradicate cancer cells via ferroptosis/apoptosis hybrid pathway. After confirming the detailed mechanism of MON-p53 in evoking ferroptosis, we further discovered that MON-p53 mediated a "bystander effect" to further sensitize cancer cells toward the MON-p53 induced ferroptosis...
December 29, 2016: Nano Letters
https://www.readbyqxmd.com/read/28012440/nrf2-inhibition-reverses-the-resistance-of-cisplatin-resistant-head-and-neck-cancer-cells-to-artesunate-induced-ferroptosis
#17
Jong-Lyel Roh, Eun Hye Kim, Hyejin Jang, Daiha Shin
Artesunate, an anti-malarial drug, has been repurposed as an anticancer drug due to its induction of cell death via reactive oxygen species (ROS) production. However, the molecular mechanisms regulating cancer cell death and the resistance of cells to artesunate remain unclear. We investigated the molecular mechanisms behind the antitumor effects of artesunate and an approach to overcome artesunate resistance in head and neck cancer (HNC). The effects of artesunate and trigonelline were tested in different HNC cell lines, including three cisplatin-resistant HNC cell lines...
April 2017: Redox Biology
https://www.readbyqxmd.com/read/27964880/role-of-gpx4-in-human-vascular-endothelial-cells-and-the-compensatory-activity-of-brown-rice-on-gpx4-ablation-condition
#18
Osamu Sakai, Toshinori Yasuzawa, Yoshie Sumikawa, Takashi Ueta, Hirotaka Imai, Akiyoshi Sawabe, Shigeru Ueshima
Oxidative stress is implicated in the pathologies of vascular endothelial cells. However, the importance of specific antioxidant enzymes in vascular endothelial cells is not fully understood. The purpose of this study was to elucidate the importance of Glutathione peroxidase 4 (GPx4), and the involvement of ferroptosis on cell death induced by GPx4 loss in human vascular endothelial cells. In addition, we examined the compensatory activity of brown rice on GPx4 ablation condition. Human umbilical vein endothelial cells were transfected with GPx4 or scramble control siRNA...
December 1, 2016: Pathophysiology: the Official Journal of the International Society for Pathophysiology
https://www.readbyqxmd.com/read/27943621/the-protective-effect-of-human-platelet-lysate-in-models-of-neurodegenerative-disease-involvement-of-the-akt-and-mek-pathways
#19
Flore Gouel, Bruce Do Van, Ming-Li Chou, Aurélie Jonneaux, Caroline Moreau, Régis Bordet, Thierry Burnouf, Jean-Christophe Devedjian, David Devos
Neurodegenerative diseases have huge economic and societal impacts, and place an immense emotional burden on patients and caregivers. Given that platelets have an essential physiological role in wound healing and tissue repair, human platelet lysates (HPLs) are being developed as a novel, effective biotherapy for neurodegenerative diseases. HPLs constitute abundant, readily accessible sources of physiological mixtures of many growth factors (GFs), with demonstrable effects on neuron survival and thus the development, maintenance, function and plasticity of the vertebrate nervous system...
December 12, 2016: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/27941671/non-canonical-cell-death-induced-by-p53
#20
REVIEW
Atul Ranjan, Tomoo Iwakuma
Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms...
December 9, 2016: International Journal of Molecular Sciences
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