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https://www.readbyqxmd.com/read/28100685/heat-stress-induces-ferroptosis-like-cell-death-in-plants
#1
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...
January 18, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28088622/reactive-oxygen-species-and-cancer-paradox-to-promote-or-to-suppress
#2
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...
January 11, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28027643/switching-apoptosis-to-ferroptosis-metal-organic-network-for-high-efficiency-anticancer-therapy
#3
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
#4
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...
December 18, 2016: 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
#5
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
#6
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
#7
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
https://www.readbyqxmd.com/read/27860262/ferroptosis-a-new-form-of-cell-death-and-its-relationships-with-tumourous-diseases
#8
REVIEW
Haitao Yu, Pengyi Guo, Xiaozai Xie, Yi Wang, Gang Chen
Ferroptosis is a newly discovered type of cell death that differs from traditional apoptosis and necrosis and results from iron-dependent lipid peroxide accumulation. Ferroptotic cell death is characterized by cytological changes, including cell volume shrinkage and increased mitochondrial membrane density. Ferroptosis can be induced by two classes of small-molecule substances known as class 1 (system Xc(-) inhibitors) and class 2 ferroptosis inducers [glutathione peroxidase 4 (GPx4) inhibitors]. In addition to these small-molecule substances, a number of drugs (e...
November 10, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27850378/740-inhibition-of-ferroptosis-as-a-neuroprotective-strategy-following-traumatic-brain-injury
#9
Elizabeth Kenny, Qin Yang, Emin Fidan, Lee Ann New, Tamil Selvan Anthonymuthu, Patrick Kochanek, Valerian Kagan, Hulya Bayir
No abstract text is available yet for this article.
December 2016: Critical Care Medicine
https://www.readbyqxmd.com/read/27836545/discovery-of-gpx4-inhibitory-peptides-from-random-peptide-t7-phage-display-and-subsequent-structural-analysis
#10
Kotaro Sakamoto, Satoshi Sogabe, Yusuke Kamada, Shin-Ichi Matsumoto, Akito Kadotani, Jun-Ichi Sakamoto, Akiyoshi Tani
The phospholipid hydroperoxidase glutathione peroxidase (GPX4) is an enzyme that reduces lipid hydroperoxides in lipid membranes. Recently, GPX4 has been investigated as a target molecule that induces iron-dependent cell death (ferroptosis) selectively in cancer cells that express mutant Ras. GPX4 inhibitors have the potential to become novel anti-cancer drugs. However, there are no druggable pockets for conventional small molecules on the molecular surface of GPX4. To generate GPX4 inhibitors, we examined the use of peptides as an alternative to small molecules...
January 8, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27793671/antiferroptotic-activity-of-non-oxidative-dopamine
#11
Ding Wang, Yingpeng Peng, Yangchun Xie, Borong Zhou, Xiaofang Sun, Rui Kang, Daolin Tang
Dopamine is a neurotransmitter that has many functions in the nervous and immune systems. Ferroptosis is a non-apoptotic form of regulated cell death that is involved in cancer and neurodegenerative diseases. However, the role of dopamine in ferroptosis remains unidentified. Here, we show that the non-oxidative form of dopamine is a strong inhibitor of ferroptotic cell death. Dopamine dose-dependently blocked ferroptosis in cancer (PANC1 and HEY) and non-cancer (MEF and HEK293) cells following treatment with erastin, a small molecule ferroptosis inducer...
October 25, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27791175/ironing-out-how-p53-regulates-ferroptosis
#12
Maureen E Murphy
No abstract text is available yet for this article.
November 1, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27777421/glutathione-peroxidase-4-a-new-player-in-neurodegeneration
#13
B R Cardoso, D J Hare, A I Bush, B R Roberts
Glutathione peroxidase 4 (GPx4) is an antioxidant enzyme reported as an inhibitor of ferroptosis, a recently discovered non-apoptotic form of cell death. This pathway was initially described in cancer cells and has since been identified in hippocampal and renal cells. In this Perspective, we propose that inhibition of ferroptosis by GPx4 provides protective mechanisms against neurodegeneration. In addition, we suggest that selenium deficiency enhances susceptibility to ferroptotic processes, as well as other programmed cell death pathways due to a reduction in GPx4 activity...
October 25, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27773819/fancd2-protects-against-bone-marrow-injury-from-ferroptosis
#14
Xinxin Song, Yangchun Xie, Rui Kang, Wen Hou, Xiaofang Sun, Michael W Epperly, Joel S Greenberger, Daolin Tang
Bone marrow injury remains a serious concern in traditional cancer treatment. Ferroptosis is an iron- and oxidative-dependent form of regulated cell death that has become part of an emerging strategy for chemotherapy. However, the key regulator of ferroptosis in bone marrow injury remains unknown. Here, we show that Fanconi anemia complementation group D2 (FANCD2), a nuclear protein involved in DNA damage repair, protects against ferroptosis-mediated injury in bone marrow stromal cells (BMSCs). The classical ferroptosis inducer erastin remarkably increased the levels of monoubiquitinated FANCD2, which in turn limited DNA damage in BMSCs...
October 20, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27768321/an-endoperoxide-reactivity-based-fret-probe-for-ratiometric-fluorescence-imaging-of-labile-iron-pools-in-living-cells
#15
Allegra T Aron, Morten O Loehr, Jana Bogena, Christopher J Chang
Iron is essential for sustaining life, as its ability to cycle between multiple oxidation states is critical for catalyzing chemical transformations in biological systems. However, without proper regulation, this same redox capacity can trigger oxidative stress events that contribute to aging along with diseases ranging from cancer to cardiovascular and neurodegenerative disorders. Despite its importance, methods for monitoring biological iron bound weakly to cellular ligands-the labile iron pool-to generate a response that preserves spatial and temporal information remain limited, owing to the potent fluorescence quenching ability of iron...
October 21, 2016: Journal of the American Chemical Society
https://www.readbyqxmd.com/read/27725964/a-mitochondrial-targeted-nitroxide-is-a-potent-inhibitor-of-ferroptosis
#16
Tanja Krainz, Michael M Gaschler, Chaemin Lim, Joshua R Sacher, Brent R Stockwell, Peter Wipf
Discovering compounds and mechanisms for inhibiting ferroptosis, a form of regulated, nonapoptotic cell death, has been of great interest in recent years. In this study, we demonstrate the ability of XJB-5-131, JP4-039, and other nitroxide-based lipid peroxidation mitigators to prevent ferroptotic cell death in HT-1080, BJeLR, and panc-1 cells. Several analogues of the reactive oxygen species (ROS) scavengers XJB-5-131 and JP4-039 were synthesized to probe structure-activity relationships and the influence of subcellular localization on the potency of these novel ferroptosis suppressors...
September 28, 2016: ACS Central Science
https://www.readbyqxmd.com/read/27705786/acetylation-is-crucial-for-p53-mediated-ferroptosis-and-tumor-suppression
#17
Shang-Jui Wang, Dawei Li, Yang Ou, Le Jiang, Yue Chen, Yingming Zhao, Wei Gu
Although previous studies indicate that loss of p53-mediated cell cycle arrest, apoptosis, and senescence does not completely abrogate its tumor suppression function, it is unclear how the remaining activities of p53 are regulated. Here, we have identified an acetylation site at lysine K98 in mouse p53 (or K101 for human p53). Whereas the loss of K98 acetylation (p53(K98R)) alone has very modest effects on p53-mediated transactivation, simultaneous mutations at all four acetylation sites (p53(4KR): K98R+ 3KR[K117R+K161R+K162R]) completely abolish its ability to regulate metabolic targets, such as TIGAR and SLC7A11...
October 4, 2016: Cell Reports
https://www.readbyqxmd.com/read/27698118/activation-of-sat1-engages-polyamine-metabolism-with-p53-mediated-ferroptotic-responses
#18
Yang Ou, Shang-Jui Wang, Dawei Li, Bo Chu, Wei Gu
Although p53-mediated cell-cycle arrest, senescence, and apoptosis remain critical barriers to cancer development, the emerging role of p53 in cell metabolism, oxidative responses, and ferroptotic cell death has been a topic of great interest. Nevertheless, it is unclear how p53 orchestrates its activities in multiple metabolic pathways into tumor suppressive effects. Here, we identified the SAT1 (spermidine/spermine N(1)-acetyltransferase 1) gene as a transcription target of p53. SAT1 is a rate-limiting enzyme in polyamine catabolism critically involved in the conversion of spermidine and spermine back to putrescine...
November 1, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27668796/ultrasmall-nanoparticles-induce-ferroptosis-in-nutrient-deprived-cancer-cells-and-suppress-tumour-growth
#19
Sung Eun Kim, Li Zhang, Kai Ma, Michelle Riegman, Feng Chen, Irina Ingold, Marcus Conrad, Melik Ziya Turker, Minghui Gao, Xuejun Jiang, Sebastien Monette, Mohan Pauliah, Mithat Gonen, Pat Zanzonico, Thomas Quinn, Ulrich Wiesner, Michelle S Bradbury, Michael Overholtzer
The design of cancer-targeting particles with precisely tuned physicochemical properties may enhance the delivery of therapeutics and access to pharmacological targets. However, a molecular-level understanding of the interactions driving the fate of nanomedicine in biological systems remains elusive. Here, we show that ultrasmall (<10 nm in diameter) poly(ethylene glycol)-coated silica nanoparticles, functionalized with melanoma-targeting peptides, can induce a form of programmed cell death known as ferroptosis in starved cancer cells and cancer-bearing mice...
November 2016: Nature Nanotechnology
https://www.readbyqxmd.com/read/27612422/temozolomide-toxicity-operates-in-a-xct-slc7a11-dependent-manner-and-is-fostered-by-ferroptosis
#20
REVIEW
Tina Sehm, Manfred Rauh, Kurt Wiendieck, Michael Buchfelder, IIker Y Eyüpoglu, Nicolai E Savaskan
The glutamate exchanger xCT (SLC7a11) is causally linked with the malignancy grade of brain tumors and represents a key player in glutamate, cystine and glutathione metabolism. Although blocking xCT is not cytotoxic for brain tumors, xCT inhibition disrupts the neurodegenerative and microenvironment-toxifying activity of gliomas. Here, we report on the use of various xCT inhibitors as single modal drugs and in combination with the autophagy-inducing standard chemotherapeutic agent temozolomide (Temodal/Temcad®, TMZ)...
September 6, 2016: Oncotarget
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