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Acetyl-CoA Synthetase 2 Promotes Acetate Utilization and Maintains Cancer Cell Growth under Metabolic Stress

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TLDR
A critical role for acetate consumption in the production of lipid biomass within the harsh tumor microenvironment is concluded, indicating a critical role in the growth of cancer cell growth under low-oxygen and lipid-depleted conditions.
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This article is published in Cancer Cell.The article was published on 2015-01-12 and is currently open access. It has received 569 citations till now. The article focuses on the topics: ACSS2 & Acetyl—CoA synthetase.

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The Emerging Hallmarks of Cancer Metabolism

TL;DR: This Perspective has organized known cancer-associated metabolic changes into six hallmarks: deregulated uptake of glucose and amino acids, use of opportunistic modes of nutrient acquisition, useof glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, increased demand for nitrogen, alterations in metabolite-driven gene regulation, and metabolic interactions with the microenvironment.
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Fundamentals of cancer metabolism

TL;DR: 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.
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Metabolic pathways promoting cancer cell survival and growth.

TL;DR: These adaptive mechanisms that promote metabolic reprogramming in cancer and emerging approaches to probe tumour metabolism in vivo are discussed and their potential to expand the metabolic repertoire of malignant cells even further are discussed.
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Cancer metabolism: a therapeutic perspective

TL;DR: How cancer cells reprogramme their metabolism and that of other cells within the tumour microenvironment in order to survive and propagate, thus driving disease progression is discussed; in particular, potential metabolic vulnerabilities that might be targeted therapeutically are highlighted.
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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.
References
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Journal ArticleDOI

The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity

TL;DR: The results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents and the generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of ‘personalized’ therapeutic regimens.
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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.
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Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis

TL;DR: FASN, a nearly-universal druggable target in many human carcinomas and their precursor lesions, offers new therapeutic opportunities for metabolically treating and preventing cancer.
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