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1. A cell state-specific metabolic vulnerability to GPX4-dependent ferroptosis in glioblastoma

Author

Banu, Matei A, Dovas, Athanassios, Argenziano, Michael G, Zhao, Wenting, Sperring, Colin P, Cuervo Grajal, Henar, Liu, Zhouzerui, Higgins, Dominique MO, Amini, Misha, Pereira, Brianna, Ye, Ling F, Mahajan, Aayushi, Humala, Nelson, Furnari, Julia L, Upadhyayula, Pavan S, Zandkarimi, Fereshteh, Nguyen, Trang TT, Teasley, Damian, Wu, Peter B, Hai, Li, Karan, Charles, Dowdy, Tyrone, Razavilar, Aida, Siegelin, Markus D, Kitajewski, Jan, Larion, Mioara, Bruce, Jeffrey N, Stockwell, Brent R, Sims, Peter A, and Canoll, Peter

Published
2024
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5. Ferroptosis in health and disease

Author

Berndt, Carsten, Alborzinia, Hamed, Amen, Vera Skafar, Ayton, Scott, Barayeu, Uladzimir, Bartelt, Alexander, Bayir, Hülya, Bebber, Christina M., Birsoy, Kivanc, Böttcher, Jan P., Brabletz, Simone, Brabletz, Thomas, Brown, Ashley R., Brüne, Bernhard, Bulli, Giorgia, Bruneau, Alix, Chen, Quan, DeNicola, Gina M., Dick, Tobias P., Distéfano, Ayelén, Dixon, Scott J., Engler, Jan B., Esser-von Bieren, Julia, Fedorova, Maria, Friedmann Angeli, José Pedro, Friese, Manuel A., Fuhrmann, Dominic C., García-Sáez, Ana J., Garbowicz, Karolina, Götz, Magdalena, Gu, Wei, Hammerich, Linda, Hassannia, Behrouz, Jiang, Xuejun, Jeridi, Aicha, Kang, Yun Pyo, Kagan, Valerian E., Konrad, David B., Kotschi, Stefan, Lei, Peng, Le Tertre, Marlène, Lev, Sima, Liang, Deguang, Linkermann, Andreas, Lohr, Carolin, Lorenz, Svenja, Luedde, Tom, Methner, Axel, Michalke, Bernhard, Milton, Anna V., Min, Junxia, Mishima, Eikan, Müller, Sebastian, Motohashi, Hozumi, Muckenthaler, Martina U., Murakami, Shohei, Olzmann, James A., Pagnussat, Gabriela, Pan, Zijan, Papagiannakopoulos, Thales, Pedrera Puentes, Lohans, Pratt, Derek A., Proneth, Bettina, Ramsauer, Lukas, Rodriguez, Raphael, Saito, Yoshiro, Schmidt, Felix, Schmitt, Carina, Schulze, Almut, Schwab, Annemarie, Schwantes, Anna, Soula, Mariluz, Spitzlberger, Benedikt, Stockwell, Brent R., Thewes, Leonie, Thorn-Seshold, Oliver, Toyokuni, Shinya, Tonnus, Wulf, Trumpp, Andreas, Vandenabeele, Peter, Vanden Berghe, Tom, Venkataramani, Vivek, Vogel, Felix C.E., von Karstedt, Silvia, Wang, Fudi, Westermann, Frank, Wientjens, Chantal, Wilhelm, Christoph, Wölk, Michele, Wu, Katherine, Yang, Xin, Yu, Fan, Zou, Yilong, and Conrad, Marcus

Published
2024
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8. Dietary restriction of cysteine and methionine sensitizes gliomas to ferroptosis and induces alterations in energetic metabolism

Author

Upadhyayula, Pavan S., Higgins, Dominique M., Mela, Angeliki, Banu, Matei, Dovas, Athanassios, Zandkarimi, Fereshteh, Patel, Purvi, Mahajan, Aayushi, Humala, Nelson, Nguyen, Trang T. T., Chaudhary, Kunal R., Liao, Lillian, Argenziano, Michael, Sudhakar, Tejaswi, Sperring, Colin P., Shapiro, Benjamin L., Ahmed, Eman R., Kinslow, Connor, Ye, Ling F., Siegelin, Markus D., Cheng, Simon, Soni, Rajesh, Bruce, Jeffrey N., Stockwell, Brent R., and Canoll, Peter

Published
2023
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9. Advances and prospects for the Human BioMolecular Atlas Program (HuBMAP)

Author

Jain, Sanjay, Pei, Liming, Spraggins, Jeffrey M., Angelo, Michael, Carson, James P., Gehlenborg, Nils, Ginty, Fiona, Gonçalves, Joana P., Hagood, James S., Hickey, John W., Kelleher, Neil L., Laurent, Louise C., Lin, Shin, Lin, Yiing, Liu, Huiping, Naba, Alexandra, Nakayasu, Ernesto S., Qian, Wei-Jun, Radtke, Andrea, Robson, Paul, Stockwell, Brent R., Van de Plas, Raf, Vlachos, Ioannis S., Zhou, Mowei, Börner, Katy, and Snyder, Michael P.

Published
2023
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15. Author Correction: Advances and prospects for the Human BioMolecular Atlas Program (HuBMAP)

Author

Jain, Sanjay, Pei, Liming, Spraggins, Jeffrey M., Angelo, Michael, Carson, James P., Gehlenborg, Nils, Ginty, Fiona, Gonçalves, Joana P., Hagood, James S., Hickey, John W., Kelleher, Neil L., Laurent, Louise C., Lin, Shin, Lin, Yiing, Liu, Huiping, Naba, Alexandra, Nakayasu, Ernesto S., Qian, Wei-Jun, Radtke, Andrea, Robson, Paul, Stockwell, Brent R., Van de Plas, Raf, Vlachos, Ioannis S., Zhou, Mowei, Börner, Katy, and Snyder, Michael P.

Published
2024
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16. Development of therapies for rare genetic disorders of GPX4: roadmap and opportunities

Author

Cheff, Dorian M, Muotri, Alysson R, Stockwell, Brent R, Schmidt, Edward E, Ran, Qitao, Kartha, Reena V, Johnson, Simon C, Mittal, Plavi, Arnér, Elias SJ, Wigby, Kristen M, Hall, Matthew D, and Ramesh, Sanath Kumar

Subjects
Rare Diseases, Genetics, Orphan Drug, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Humans, Osteochondrodysplasias, Sedaghatian-type spondylometaphyseal dysplasia, SSMD, Glutathione peroxidase 4, GPX4, Rare genetic disorder, Therapy development, Roadmap, Ultra-rare disease, Other Medical and Health Sciences, Genetics & Heredity
Abstract

BackgroundExtremely rare progressive diseases like Sedaghatian-type Spondylometaphyseal Dysplasia (SSMD) can be neonatally lethal and therefore go undiagnosed or are difficult to treat. Recent sequencing efforts have linked this disease to mutations in GPX4, with consequences in the resulting enzyme, glutathione peroxidase 4. This offers potential diagnostic and therapeutic avenues for those suffering from this disease, though the steps toward these treatments is often convoluted, expensive, and time-consuming.Main bodyThe CureGPX4 organization was developed to promote awareness of GPX4-related diseases like SSMD, as well as support research that could lead to essential therapeutics for patients. We provide an overview of the 21 published SSMD cases and have compiled additional sequencing data for four previously unpublished individuals to illustrate the genetic component of SSMD, and the role of sequencing data in diagnosis. We outline in detail the steps CureGPX4 has taken to reach milestones of team creation, disease understanding, drug repurposing, and design of future studies.ConclusionThe primary aim of this review is to provide a roadmap for therapy development for rare, ultra-rare, and difficult to diagnose diseases, as well as increase awareness of the genetic component of SSMD. This work will offer a better understanding of GPx4-related diseases, and help guide researchers, clinicians, and patients interested in other rare diseases find a path towards treatments.

Published
2021

20. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco E., Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K. -M., Chen, Guo-Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, Bart, Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravichandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe S., Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strapazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, Gyorgy, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, Alexei, Villunger, Andreas, von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Huang-Tian, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibing, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Published
2023
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22. Promotion of cholangiocarcinoma growth by diverse cancer-associated fibroblast subpopulations

Author

Affo, Silvia, Nair, Ajay, Brundu, Francesco, Ravichandra, Aashreya, Bhattacharjee, Sonakshi, Matsuda, Michitaka, Chin, LiKang, Filliol, Aveline, Wen, Wen, Song, Xinhua, Decker, Aubrianna, Worley, Jeremy, Caviglia, Jorge Matias, Yu, Lexing, Yin, Deqi, Saito, Yoshinobu, Savage, Thomas, Wells, Rebecca G, Mack, Matthias, Zender, Lars, Arpaia, Nicholas, Remotti, Helen E, Rabadan, Raul, Sims, Peter, Leblond, Anne-Laure, Weber, Achim, Riener, Marc-Oliver, Stockwell, Brent R, Gaublomme, Jellert, Llovet, Josep M, Kalluri, Raghu, Michalopoulos, George K, Seki, Ekihiro, Sia, Daniela, Chen, Xin, Califano, Andrea, and Schwabe, Robert F

Subjects
Genetics, Liver Disease, Cancer, Digestive Diseases - (Gallbladder), Chronic Liver Disease and Cirrhosis, Digestive Diseases, Liver Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Aged, Animals, Bile Duct Neoplasms, Bile Ducts, Intrahepatic, Cancer-Associated Fibroblasts, Cholangiocarcinoma, Collagen Type I, Female, Hepatic Stellate Cells, Hepatocyte Growth Factor, Humans, Hyaluronan Synthases, Hyaluronic Acid, Male, Mice, Transgenic, Middle Aged, Proto-Oncogene Proteins c-met, Tumor Microenvironment, CellPhoneDB, HGF, KRAS, YAP, cholangiocarcinoma, immune, mechanosensitive, single cell, stiffness, tumor microenvironment, Neurosciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Cancer-associated fibroblasts (CAF) are a poorly characterized cell population in the context of liver cancer. Our study investigates CAF functions in intrahepatic cholangiocarcinoma (ICC), a highly desmoplastic liver tumor. Genetic tracing, single-cell RNA sequencing, and ligand-receptor analyses uncovered hepatic stellate cells (HSC) as the main source of CAF and HSC-derived CAF as the dominant population interacting with tumor cells. In mice, CAF promotes ICC progression, as revealed by HSC-selective CAF depletion. In patients, a high panCAF signature is associated with decreased survival and increased recurrence. Single-cell RNA sequencing segregates CAF into inflammatory and growth factor-enriched (iCAF) and myofibroblastic (myCAF) subpopulations, displaying distinct ligand-receptor interactions. myCAF-expressed hyaluronan synthase 2, but not type I collagen, promotes ICC. iCAF-expressed hepatocyte growth factor enhances ICC growth via tumor-expressed MET, thus directly linking CAF to tumor cells. In summary, our data demonstrate promotion of desmoplastic ICC growth by therapeutically targetable CAF subtype-specific mediators, but not by type I collagen.

Published
2021

24. Resolving the paradox of ferroptotic cell death: Ferrostatin-1 binds to 15LOX/PEBP1 complex, suppresses generation of peroxidized ETE-PE, and protects against ferroptosis

Author

Anthonymuthu, Tamil S, Tyurina, Yulia Y, Sun, Wan-Yang, Mikulska-Ruminska, Karolina, Shrivastava, Indira H, Tyurin, Vladimir A, Cinemre, Fatma B, Dar, Haider H, VanDemark, Andrew P, Holman, Theodore R, Sadovsky, Yoel, Stockwell, Brent R, He, Rong-Rong, Bahar, Ivet, Bayır, Hülya, and Kagan, Valerian E

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cell Death, Cyclohexylamines, Ferroptosis, Oxidation-Reduction, Phenylenediamines, Ferrostatin-1, 15-Lipoxygenase, Hydroperoxy-eicosatetraenoyl-phosphatidylethanolamines, Phospholipid peroxidation, Medical Biochemistry and Metabolomics, Pharmacology and Pharmaceutical Sciences, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

Hydroperoxy-eicosatetraenoyl-phosphatidylethanolamine (HpETE-PE) is a ferroptotic cell death signal. HpETE-PE is produced by the 15-Lipoxygenase (15LOX)/Phosphatidylethanolamine Binding Protein-1 (PEBP1) complex or via an Fe-catalyzed non-enzymatic radical reaction. Ferrostatin-1 (Fer-1), a common ferroptosis inhibitor, is a lipophilic radical scavenger but a poor 15LOX inhibitor arguing against 15LOX having a role in ferroptosis. In the current work, we demonstrate that Fer-1 does not affect 15LOX alone, however, it effectively inhibits HpETE-PE production by the 15LOX/PEBP1 complex. Computational molecular modeling shows that Fer-1 binds to the 15LOX/PEBP1 complex at three sites and could disrupt the catalytically required allosteric motions of the 15LOX/PEBP1 complex. Using nine ferroptosis cell/tissue models, we show that HpETE-PE is produced by the 15LOX/PEBP1 complex and resolve the long-existing Fer-1 anti-ferroptotic paradox.

Published
2021

27. MDM2 and MDMX promote ferroptosis by PPARα-mediated lipid remodeling

Author

Venkatesh, Divya, O'Brien, Nicholas A, Zandkarimi, Fereshteh, Tong, David R, Stokes, Michael E, Dunn, Denise E, Kengmana, Everett S, Aron, Allegra T, Klein, Alyssa M, Csuka, Joleen M, Moon, Sung-Hwan, Conrad, Marcus, Chang, Christopher J, Lo, Donald C, D'Alessandro, Angelo, Prives, Carol, and Stockwell, Brent R

Subjects
Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Generic health relevance, Animals, Brain, Cell Cycle Proteins, Ferroptosis, Glioblastoma, HCT116 Cells, Humans, Lipid Metabolism, Mutation, PPAR alpha, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-mdm2, RNA Interference, Rats, Tumor Suppressor Protein p53, Ubiquinone, ferroptosis, MDM2, MDMX, p53-independent, lipid metabolism, FSP1, CoQ(10), cancer, CoQ10, PPARα, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental Biology
Abstract

MDM2 and MDMX, negative regulators of the tumor suppressor p53, can work separately and as a heteromeric complex to restrain p53's functions. MDM2 also has pro-oncogenic roles in cells, tissues, and animals that are independent of p53. There is less information available about p53-independent roles of MDMX or the MDM2-MDMX complex. We found that MDM2 and MDMX facilitate ferroptosis in cells with or without p53. Using small molecules, RNA interference reagents, and mutant forms of MDMX, we found that MDM2 and MDMX, likely working in part as a complex, normally facilitate ferroptotic death. We observed that MDM2 and MDMX alter the lipid profile of cells to favor ferroptosis. Inhibition of MDM2 or MDMX leads to increased levels of FSP1 protein and a consequent increase in the levels of coenzyme Q10, an endogenous lipophilic antioxidant. This suggests that MDM2 and MDMX normally prevent cells from mounting an adequate defense against lipid peroxidation and thereby promote ferroptosis. Moreover, we found that PPARα activity is essential for MDM2 and MDMX to promote ferroptosis, suggesting that the MDM2-MDMX complex regulates lipids through altering PPARα activity. These findings reveal the complexity of cellular responses to MDM2 and MDMX and suggest that MDM2-MDMX inhibition might be useful for preventing degenerative diseases involving ferroptosis. Furthermore, they suggest that MDM2/MDMX amplification may predict sensitivity of some cancers to ferroptosis inducers.

Published
2020

28. Leveraging insights into cancer metabolism—a symposium report

Author

Cable, Jennifer, Finley, Lydia, Tu, Benjamin P, Patti, Gary J, Oliver, Trudy G, Vardhana, Santosha, Mana, Miyeko, Ericksen, Russell, Khare, Sanika, DeBerardinis, Ralph, Stockwell, Brent R, Edinger, Aimee, Haigis, Marcia, and Kaelin, William

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Cell Transformation, Neoplastic, Congresses as Topic, Energy Metabolism, Humans, Metabolic Networks and Pathways, Neoplasms, New York City, Research Report, cancer, cell signaling, ferroptosis, micropinocytosis, metabolism, General Science & Technology
Abstract

Tumor cells have devised unique metabolic strategies to garner enough nutrients to sustain continuous growth and cell division. Oncogenic mutations may alter metabolic pathways to unlock new sources of energy, and cells take the advantage of various scavenging pathways to ingest material from their environment. These changes in metabolism result in a metabolic profile that, in addition to providing the building blocks for macromolecules, can also influence cell signaling pathways to promote tumor initiation and progression. Understanding what pathways tumor cells use to synthesize the materials necessary to support metabolic growth can pave the way for new cancer therapeutics. Potential strategies include depriving tumors of the materials needed to grow or targeting pathways involved in dependencies that arise by virtue of their altered metabolis.

Published
2020

29. Ferroptosis regulates hemolysis in stored murine and human red blood cells

Author

D'Alessandro, Angelo, primary, Keele, Gregory R, additional, Hay, Ariel, additional, Nemkov, Travis, additional, Earley, Eric Jay, additional, Stephenson, Daniel, additional, Vincent, Matthew, additional, Deng, Xutao, additional, Stone, Mars, additional, Dzieciatkowska, Monika, additional, Hansen, Kirk, additional, Kleinman, Steve, additional, Spitalnik, Steven L, additional, Roubinian, Nareg, additional, Norris, Philip J, additional, Busch, Michael P, additional, Page, Grier P, additional, Stockwell, Brent R, additional, Churchill, Gary A, additional, and Zimring, James C, additional

Published
2024
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32. Development of optimized drug-like small molecule inhibitors of the SARS-CoV-2 3CL protease for treatment of COVID-19

Author

Liu, Hengrui, Iketani, Sho, Zask, Arie, Khanizeman, Nisha, Bednarova, Eva, Forouhar, Farhad, Fowler, Brandon, Hong, Seo Jung, Mohri, Hiroshi, Nair, Manoj S., Huang, Yaoxing, Tay, Nicholas E. S., Lee, Sumin, Karan, Charles, Resnick, Samuel J., Quinn, Colette, Li, Wenjing, Shion, Henry, Xia, Xin, Daniels, Jacob D., Bartolo-Cruz, Michelle, Farina, Marcelo, Rajbhandari, Presha, Jurtschenko, Christopher, Lauber, Matthew A., McDonald, Thomas, Stokes, Michael E., Hurst, Brett L., Rovis, Tomislav, Chavez, Alejandro, Ho, David D., and Stockwell, Brent R.

Published
2022
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33. Klebsiella pneumoniae induces host metabolic stress that promotes tolerance to pulmonary infection

Author

Wong Fok Lung, Tania, Charytonowicz, Daniel, Beaumont, Kristin G., Shah, Shivang S., Sridhar, Shwetha H., Gorrie, Claire L., Mu, Andre, Hofstaedter, Casey E., Varisco, David, McConville, Thomas H., Drikic, Marija, Fowler, Brandon, Urso, Andreacarola, Shi, Wei, Fucich, Dario, Annavajhala, Medini K., Khan, Ibrahim N., Oussenko, Irina, Francoeur, Nancy, Smith, Melissa L., Stockwell, Brent R., Lewis, Ian A., Hachani, Abderrahman, Upadhyay Baskota, Swikrity, Uhlemann, Anne-Catrin, Ahn, Danielle, Ernst, Robert K., Howden, Benjamin P., Sebra, Robert, and Prince, Alice

Published
2022
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34. Proteomic analysis of ferroptosis pathways reveals a role of CEPT1 in suppressing ferroptosis.

Author

Liu, Xiaoguang, Chen, Zhen, Yan, Yuelong, Zandkarimi, Fereshteh, Nie, Litong, Li, Qidong, Horbath, Amber, Olszewski, Kellen, Kondiparthi, Lavanya, Mao, Chao, Lee, Hyemin, Zhuang, Li, Poyurovsky, Masha, Stockwell, Brent R, Chen, Junjie, and Gan, Boyi

Abstract

Ferroptosis has been recognized as a unique cell death modality driven by excessive lipid peroxidation and unbalanced cellular metabolism. In this study, we established a protein interaction landscape for ferroptosis pathways through proteomic analyses, and identified choline/ethanolamine phosphotransferase 1 (CEPT1) as a lysophosphatidylcholine acyltransferase 3 (LPCAT3)-interacting protein that regulates LPCAT3 protein stability. In contrast to its known role in promoting phospholipid synthesis, we showed that CEPT1 suppresses ferroptosis potentially by interacting with phospholipases and breaking down certain pro-ferroptotic polyunsaturated fatty acid (PUFA)-containing phospholipids. Together, our study reveals a previously unrecognized role of CEPT1 in suppressing ferroptosis. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Dependency of a therapy-resistant state of cancer cells on a lipid peroxidase pathway

Author

Viswanathan, Vasanthi S, Ryan, Matthew J, Dhruv, Harshil D, Gill, Shubhroz, Eichhoff, Ossia M, Seashore-Ludlow, Brinton, Kaffenberger, Samuel D, Eaton, John K, Shimada, Kenichi, Aguirre, Andrew J, Viswanathan, Srinivas R, Chattopadhyay, Shrikanta, Tamayo, Pablo, Yang, Wan Seok, Rees, Matthew G, Chen, Sixun, Boskovic, Zarko V, Javaid, Sarah, Huang, Cherrie, Wu, Xiaoyun, Tseng, Yuen-Yi, Roider, Elisabeth M, Gao, Dong, Cleary, James M, Wolpin, Brian M, Mesirov, Jill P, Haber, Daniel A, Engelman, Jeffrey A, Boehm, Jesse S, Kotz, Joanne D, Hon, Cindy S, Chen, Yu, Hahn, William C, Levesque, Mitchell P, Doench, John G, Berens, Michael E, Shamji, Alykhan F, Clemons, Paul A, Stockwell, Brent R, and Schreiber, Stuart L

Subjects
Cancer, Cadherins, Cell Death, Cell Line, Tumor, Cell Lineage, Cell Transdifferentiation, Drug Resistance, Neoplasm, Epithelial-Mesenchymal Transition, Glutathione Peroxidase, Humans, Iron, Lipid Peroxidation, Lipid Peroxides, Male, Melanoma, Mesoderm, Neoplasms, Phospholipid Hydroperoxide Glutathione Peroxidase, Prostatic Neoplasms, Proteomics, Proto-Oncogene Proteins B-raf, Reproducibility of Results, Zinc Finger E-box-Binding Homeobox 1, General Science & Technology
Abstract

Plasticity of the cell state has been proposed to drive resistance to multiple classes of cancer therapies, thereby limiting their effectiveness. A high-mesenchymal cell state observed in human tumours and cancer cell lines has been associated with resistance to multiple treatment modalities across diverse cancer lineages, but the mechanistic underpinning for this state has remained incompletely understood. Here we molecularly characterize this therapy-resistant high-mesenchymal cell state in human cancer cell lines and organoids and show that it depends on a druggable lipid-peroxidase pathway that protects against ferroptosis, a non-apoptotic form of cell death induced by the build-up of toxic lipid peroxides. We show that this cell state is characterized by activity of enzymes that promote the synthesis of polyunsaturated lipids. These lipids are the substrates for lipid peroxidation by lipoxygenase enzymes. This lipid metabolism creates a dependency on pathways converging on the phospholipid glutathione peroxidase (GPX4), a selenocysteine-containing enzyme that dissipates lipid peroxides and thereby prevents the iron-mediated reactions of peroxides that induce ferroptotic cell death. Dependency on GPX4 was found to exist across diverse therapy-resistant states characterized by high expression of ZEB1, including epithelial-mesenchymal transition in epithelial-derived carcinomas, TGFβ-mediated therapy-resistance in melanoma, treatment-induced neuroendocrine transdifferentiation in prostate cancer, and sarcomas, which are fixed in a mesenchymal state owing to their cells of origin. We identify vulnerability to ferroptic cell death induced by inhibition of a lipid peroxidase pathway as a feature of therapy-resistant cancer cells across diverse mesenchymal cell-state contexts.

Published
2017

38. A guideline on the molecular ecosystem regulating ferroptosis

Author

Dai, Enyong, Chen, Xin, Linkermann, Andreas, Jiang, Xuejun, Kang, Rui, Kagan, Valerian E., Bayir, Hülya, Yang, Wan Seok, Garcia-Saez, Ana J., Ioannou, Maria S., Janowitz, Tobias, Ran, Qitao, Gu, Wei, Gan, Boyi, Krysko, Dmitri V., Zhu, Xiaofeng, Wang, Jiayi, Krautwald, Stefan, Toyokuni, Shinya, Xie, Yangchun, Greten, Florian R., Yi, Qing, Schick, Joel, Liu, Jiao, Gabrilovich, Dmitry I., Liu, Jinbao, Zeh, Herbert J., Zhang, Donna D., Yang, Minghua, Iovanna, Juan, Kopf, Manfred, Adolph, Timon E., Chi, Jen-Tsan, Li, Changfeng, Ichijo, Hidenori, Karin, Michael, Sankaran, Vijay G., Zou, Weiping, Galluzzi, Lorenzo, Bush, Ashley I., Li, Binghui, Melino, Gerry, Baehrecke, Eric H., Lotze, Michael T., Klionsky, Daniel J., Stockwell, Brent R., Kroemer, Guido, and Tang, Daolin

Abstract

Ferroptosis, an intricately regulated form of cell death characterized by uncontrolled lipid peroxidation, has garnered substantial interest since this term was first coined in 2012. Recent years have witnessed remarkable progress in elucidating the detailed molecular mechanisms that govern ferroptosis induction and defence, with particular emphasis on the roles of heterogeneity and plasticity. In this Review, we discuss the molecular ecosystem of ferroptosis, with implications that may inform and enable safe and effective therapeutic strategies across a broad spectrum of diseases.

Published
2024
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39. Ferroptosis and aerobic training in ageing: A review

Author

Kordi, Negin, Saydi, Ali, Karami, Sajad, Bagherzadeh-Rahmani, Behnam, Marzetti, Emanuele, Jung, Friedrich, Stockwell, Brent R., Marzetti, Emanuele (ORCID:0000-0001-9567-6983), Kordi, Negin, Saydi, Ali, Karami, Sajad, Bagherzadeh-Rahmani, Behnam, Marzetti, Emanuele, Jung, Friedrich, Stockwell, Brent R., and Marzetti, Emanuele (ORCID:0000-0001-9567-6983)

Abstract

Ferroptosis is a form of programmed cell death that plays a significant role in causing several diseases such as heart attack and heart failure, through alterations in fat, amino acid, and iron metabolism. Comprehending the regulatory mechanisms of ferroptosis signaling is critical because it has a considerable effect on the elderly's mortality. Conversely, age-related changes in substrate metabolism and metabolite levels are recognized to give rise to obesity. Furthermore, research has proposed that aging and obesity-related changes in substrate metabolism may aggravate ferroptosis. The suppression of ferroptosis holds potential as a successful therapeutic approach for managing different diseases, including sarcopenia, cardiovascular diseases, and central nervous system diseases. However, the pathologic and biological mechanisms behind the function of ferroptosis are not fully comprehended yet. Physical activity could affect lipid, amino acid, and iron metabolism to modulate ferroptosis. The aim of this study is to showcase the current understanding of the molecular mechanisms leading to ferroptosis and discuss the role of aging and physical activity in this phenomenon.

Published
2024

42. Ferroptosis and aerobic training in ageing.

Author

Kordi, Negin, Saydi, Ali, Karami, Sajad, Bagherzadeh-Rahmani, Behnam, Marzetti, Emanuele, Jung, Friedrich, and Stockwell, Brent R.

Subjects
AMINO acid metabolism, IRON metabolism, CENTRAL nervous system diseases, APOPTOSIS, LIPID metabolism
Abstract

Ferroptosis is a form of programmed cell death that plays a significant role in causing several diseases such as heart attack and heart failure, through alterations in fat, amino acid, and iron metabolism. Comprehending the regulatory mechanisms of ferroptosis signaling is critical because it has a considerable effect on the elderly's mortality. Conversely, age-related changes in substrate metabolism and metabolite levels are recognized to give rise to obesity. Furthermore, research has proposed that aging and obesity-related changes in substrate metabolism may aggravate ferroptosis. The suppression of ferroptosis holds potential as a successful therapeutic approach for managing different diseases, including sarcopenia, cardiovascular diseases, and central nervous system diseases. However, the pathologic and biological mechanisms behind the function of ferroptosis are not fully comprehended yet. Physical activity could affect lipid, amino acid, and iron metabolism to modulate ferroptosis. The aim of this study is to showcase the current understanding of the molecular mechanisms leading to ferroptosis and discuss the role of aging and physical activity in this phenomenon. [ABSTRACT FROM AUTHOR]

Published
2024
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44. Transferrin Receptor Is a Specific Ferroptosis Marker

Author

Feng, Huizhong, Schorpp, Kenji, Jin, Jenny, Yozwiak, Carrie E., Hoffstrom, Benjamin G., Decker, Aubrianna M., Rajbhandari, Presha, Stokes, Michael E., Bender, Hannah G., Csuka, Joleen M., Upadhyayula, Pavan S., Canoll, Peter, Uchida, Koji, Soni, Rajesh K., Hadian, Kamyar, and Stockwell, Brent R.

Published
2020
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45. Subtype-selective prenylated isoflavonoids disrupt regulatory drivers of MYCN-amplified cancers

Author

Stokes, Michael E., primary, Vasciaveo, Alessandro, additional, Small, Jonnell Candice, additional, Zask, Arie, additional, Reznik, Eduard, additional, Smith, Nailah, additional, Wang, Qian, additional, Daniels, Jacob, additional, Forouhar, Farhad, additional, Rajbhandari, Presha, additional, Califano, Andrea, additional, and Stockwell, Brent R., additional

Published
2023
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50. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. 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M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. 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G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

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