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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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Induced-Decay of Glycine Decarboxylase Transcripts as an Anticancer Therapeutic Strategy for Non-Small-Cell Lung Carcinoma.

TL;DR: In this article, splicing-modulating steric hindrance antisense oligonucleotides (shAONs) are used to induce exon skipping (half maximal inhibitory concentration [IC 50 ] at 3.5-7 nM), disrupt the open reading frame (ORF) of GLDC transcript (predising it for nonsense-mediated decay), halt cell proliferation, and prevent colony formation in both A549 cells and TIC-enriched NSCLC tumor sphere cells (TS32).
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Serine racemase enhances growth of colorectal cancer by producing pyruvate from serine.

TL;DR: Serine racemase is shown to support colon-cancer growth, highlighting a new strategy that cancer cells use to maintain cellular pyruvate levels and mitochondrial mass and suggesting that SRR might be a molecular target for colorectal-cancer therapy.
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L-arginine/5-fluorouracil combination treatment approaches cells selectively: Rescuing endothelial cells while killing MDA-MB-468 breast cancer cells

TL;DR: Findings clearly suggest that L-arginine inhibits cell death induced by 5-FU in HUVECs through attenuating the adverse effects of5-FU, while it does not do so in breast cancer cells.
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Mechanism-Specific Pharmacodynamics of a Novel Complex-I Inhibitor Quantified by Imaging Reversal of Consumptive Hypoxia with [18F]FAZA PET In Vivo

TL;DR: 18F-fluoroazomycin arabinoside ([18F]FAZA), a 2-nitroimidazole-based hypoxia PET imaging agent, was combined with a rigorous test-retest imaging method for non-invasive quantification of the reversal of consumptive Hypoxia in vivo as a mechanism-specific pharmacodynamic (PD) biomarker of target engagement for IACS-010759.
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The multifaceted role of NRF2 in cancer progression and cancer stem cells maintenance

TL;DR: In this paper, the role of NRF2 in cancer stem cells (CSCs), a small population of tumor cells responsible for therapy resistance and tumor relapse, 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.
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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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