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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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Reactive oxygen species (ROS) as pleiotropic physiological signalling agents.

TL;DR: This work focuses on ROS at physiological levels and their central role in redox signalling via different post-translational modifications, denoted as ‘oxidative eustress’.
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Understanding the Intersections between Metabolism and Cancer Biology

TL;DR: In this paper, the authors define pathways that are limiting for cancer progression and understand the context specificity of metabolic preferences and liabilities in malignant cells, which can guide the more effective targeting of metabolism to help patients.
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Mitochondrial TCA cycle metabolites control physiology and disease.

TL;DR: This review summarizes the mechanisms by which the abundance of different TCA cycle metabolites controls cellular function and fate in different contexts and focuses on how these metabolites mediated signaling can affect physiology and disease.
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Mitochondria-Targeted Triphenylphosphonium-Based Compounds: Syntheses, Mechanisms of Action, and Therapeutic and Diagnostic Applications

TL;DR: The physicochemical basis for mitochondrial accumulation of lipophilic cations, synthetic chemistry strategies to target compounds to mitochondria, mitochondrial probes, and sensors, and examples of mitochondrial targeting of bioactive compounds are described.
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The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism

TL;DR: The PI3K–AKT signalling network is discussed and its control of cancer cell metabolism through both direct and indirect regulation of nutrient transport and metabolic enzymes, thereby connecting oncogenic signalling and metabolic reprogramming to support cancer cell survival and proliferation.
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.
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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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