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Open AccessJournal ArticleDOI

Fundamentals of cancer metabolism

TLDR
A conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis will progressively support the development of new strategies to treat human cancer.
Abstract
Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.

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Targeting SLC25A10 alleviates improved antioxidant capacity and associated radioresistance of cancer cells induced by chronic-cycling hypoxia.

TL;DR: A role of SLC25A10 is revealed in supporting both, redox- and energy-homeostasis, ensuring radioresistance of cancer cells with tolerance to chronic-cycling hypoxia thereby proposing a novel strategy to overcome a mechanism of hypoxIA-induced therapy resistance with potential clinical relevance regarding decreased patient survival.
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The relevance of tyrosine kinase inhibitors for global metabolic pathways in cancer.

TL;DR: This review discusses recent observations related to TKs-associated metabolism and to metabolic feedback that is initialized as cellular response to particular TK-targeted therapies, providing collective evidence that therapeutic responses are primarily linked to such pathways as regulation of lipid and amino acid metabolism, TCA cycle and glycolysis.
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The Pathophysiological Role of CoA.

TL;DR: The current knowledge of coenzyme A subcellular concentrations; the roles of CoA synthesis and degradation processes; and protein modification by reversible CoA binding to proteins (CoAlation) are summarized.
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Oncogene-regulated release of extracellular vesicles

TL;DR: In this article, the authors show that specific oncogenes reduce the biomass of cancer cells by promoting extracellular vesicle (EV) release, and they identify an inverse relationship between upregulation and activation of the RAS/MEK/ERK signaling pathway for regulating EV release in some tumor cells.
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O-GlcNAcylation and chromatin remodeling in mammals: an up-to-date overview.

TL;DR: The recent findings on the link between OGT, OGA and chromatin regulators in mammalian cellular models are summarized, and their relevance in physiological and pathological conditions is discussed.
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
Journal ArticleDOI

On the origin of cancer cells.

Origin of cancer cells

Otto Warburg
Journal ArticleDOI

How mitochondria produce reactive oxygen species.

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

mTOR Signaling in Growth Control and Disease

TL;DR: The mechanistic target of rapamycin (mTOR) signaling pathway senses and integrates a variety of environmental cues to regulate organismal growth and homeostasis as mentioned in this paper, and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration.
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