The biology of cancer: metabolic reprogramming fuels cell growth and proliferation
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TLDR
This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types and regulates regulation of these fluxes by cellular mediators of signal transduction and gene expression.About:
This article is published in Cell Metabolism.The article was published on 2008-01-01 and is currently open access. It has received 3526 citations till now. The article focuses on the topics: PI3K/AKT/mTOR pathway & Lipid biosynthesis.read more
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Recent Progress of Rare-Earth Doped Upconversion Nanoparticles: Synthesis, Optimization, and Applications.
TL;DR: The state‐of‐the‐art approaches to synthesize UCNPs in the past few years are introduced, followed by a summary of several strategies to optimize upconversion emissive properties and various applications ofUCNPs.
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Estrogen-related receptor-α is a metabolic regulator of effector T-cell activation and differentiation
Ryan D. Michalek,Valerie A. Gerriets,Amanda G. Nichols,Makoto Inoue,Dmitri Kazmin,Ching-Yi Chang,Mary A. Dwyer,Erik R. Nelson,Kristen N. Pollizzi,Olga Ilkayeva,Vincent Giguère,William J. Zuercher,Jonathan D. Powell,Mari L. Shinohara,Donald P. McDonnell,Jeffrey C. Rathmell +15 more
TL;DR: In vivo inhibition of ERRα reduced T-cell proliferation and Teff generation in both immunization and experimental autoimmune encephalomyelitis models, suggesting that ERR α is a selective transcriptional regulator of Teff metabolism that may provide a metabolic means to modulate immunity.
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Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells.
Esther Hulleman,Karin M. Kazemier,Amy Holleman,David J. VanderWeele,Charles M. Rudin,Mathilde J.C. Broekhuis,William E. Evans,Rob Pieters,Monique L. den Boer +8 more
TL;DR: It is shown that prednisolone resistance is associated with increased glucose consumption and that inhibition of glycolysis sensitizes prednisOLone-resistant ALL cell lines to glucocorticoids, and that targeting glyCOlysis is a viable strategy for modulating prednisoone resistance in ALL.
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MUC1 mucin stabilizes and activates hypoxia-inducible factor 1 alpha to regulate metabolism in pancreatic cancer
Nina V. Chaika,Teklab Gebregiworgis,Michelle E. Lewallen,Vinee Purohit,Prakash Radhakrishnan,Xiang Liu,Bo Zhang,Kamiya Mehla,Roger B. Brown,Thomas C. Caffrey,Fang Yu,Keith R. Johnson,Robert Powers,Michael A. Hollingsworth,Pankaj K. Singh +14 more
TL;DR: It is demonstrated that MUC1, a large, type I transmembrane protein that is overexpressed in several carcinomas including pancreatic adenocarcinoma, modulates cancer cell metabolism to facilitate growth properties of cancer cells.
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Mitochondrial reactive oxygen species promote p65 nuclear translocation mediating high-phosphate-induced vascular calcification in vitro and in vivo.
TL;DR: In a rat model of dietary adenine-induced chronic renal failure, MnTMPyP reduced aortic ROS levels, p65 activation, and calcium deposition, and mitochondrial ROS-mediated p65 nuclear translocation is involved in phosphate-induced VC.
References
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HIF-1-mediated expression of pyruvate dehydrogenase kinase: A metabolic switch required for cellular adaptation to hypoxia
TL;DR: A hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production is revealed.