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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.
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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.

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Fulfilling the metabolic requirements for cell proliferation.

TL;DR: The differential regulation of the activity of these proteins indicates that a finely-tuned set of mechanisms is activated to fulfil specific metabolic demands at different stages of the cell cycle, implications for the understanding of cell proliferation in general and, in particular, of cancer, its prevention and treatment.
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NAMPT overexpression induces cancer stemness and defines a novel tumor signature for glioma prognosis

TL;DR: It is reported that NAMPT overexpression in glioma cell lines increases tumorigenic properties controlling stem cell pathways and enriching the cancer-initiating cell (CIC) population and represents a novel therapeutic target in Glioma progression and relapse.
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Activation of Akt is essential for the propagation of mitochondrial respiratory stress signaling and activation of the transcriptional coactivator heterogeneous ribonucleoprotein A2.

TL;DR: It is shown that mitochondrial respiratory dysfunction activates a stress signaling that induces Akt1 activation that occurs through calcineurin-mediated IGF1R/PI3-K pathway.
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The influence of ligand organization on the rate of uptake of gold nanoparticles by colorectal cancer cells

TL;DR: The uptake of different hydrophilic mono- and dual-ligand gold nanoparticles in colorectal cancer cells in vitro is explored and it is found that the rate of uptake is dependent on the structural organization of the ligands on the surface of the particles rather than their charge or chemical properties.
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IL-37 Attenuates Lung Fibrosis by Inducing Autophagy and Regulating TGF-β1 Production in Mice.

TL;DR: Findings suggested that a decrease in IL-37 may be involved in the progression of IPF and thatIL-37 inhibited TGF-β1 signaling and enhancement of autophagy in IPF fibroblasts, and could be a therapeutic target in fibrotic lung diseases, including IPF.
References
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Journal ArticleDOI

On the origin of cancer cells.

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Targeting HIF-1 for cancer therapy

TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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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.