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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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Emerging mechanisms and targeted therapy of ferroptosis in cancer

TL;DR: Ferroptosis is an iron and lipid reactive oxygen species (ROS)-dependent form of programmed cell death that is distinct from other forms of regulatory cell death at morphological, biological, and genetic levels as discussed by the authors.
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The role of glutaminase in cancer

TL;DR: The role of glutaminase in cancer, primarily focusing on breast cancer, is explored, and the role played by oncogenes and tumour suppressor genes in regulating glutaminases is addressed, and current therapeutic approaches to targeting glutamine metabolism are discussed.
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Glucose Transporter 1-Dependent Glycolysis Is Increased during Aging-Related Lung Fibrosis, and Phloretin Inhibits Lung Fibrosis

TL;DR: It is demonstrated that the activation of AMP‐activated protein kinase, which is regulated by GLUT1‐dependent glycolysis, represents a critical metabolic pathway for fibroblast activation and is a potential target of therapy of age‐related lung fibrosis.
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Succinate: An initiator in tumorigenesis and progression.

TL;DR: How the high concentration of succinate in the tumor microenvironment acts as an active participant in tumorigenesis, rather than a passive bystander or innocent victim, and that investigational drugs with different molecular targets may expand the horizon in anticancer therapy.
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Metabolic Reprogramming and Dependencies Associated with Epithelial Cancer Stem Cells Independent of the Epithelial-Mesenchymal Transition Program.

TL;DR: It is found that the e‐CSC program in this cellular model is characterized by a high plasticity in energy substrate metabolism, including an enhanced Warburg effect, a greater carbon and energy source flexibility driven by fatty acids and amino acid metabolism and an essential reliance on the proton buffering capacity conferred by glutamine metabolism.
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.