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Mitochondria and cancer

Douglas C. Wallace
- 01 Oct 2012 - 
- Vol. 12, Iss: 10, pp 685-698
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TLDR
Cancer cells then reprogramme adjacent stromal cells to optimize the cancer cell environment and activate out-of-context programmes that are important in development, stress response, wound healing and nutritional status.
Abstract
Contrary to conventional wisdom, functional mitochondria are essential for the cancer cell. Although mutations in mitochondrial genes are common in cancer cells, they do not inactivate mitochondrial energy metabolism but rather alter the mitochondrial bioenergetic and biosynthetic state. These states communicate with the nucleus through mitochondrial 'retrograde signalling' to modulate signal transduction pathways, transcriptional circuits and chromatin structure to meet the perceived mitochondrial and nuclear requirements of the cancer cell. Cancer cells then reprogramme adjacent stromal cells to optimize the cancer cell environment. These alterations activate out-of-context programmes that are important in development, stress response, wound healing and nutritional status.

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Citations
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Mitochondrial DNA Stress Primes the Antiviral Innate Immune Response

TL;DR: It is shown that moderate mtDNA stress elicited by TFAM deficiency engages cytosolic antiviral signalling to enhance the expression of a subset of interferon-stimulated genes, and it is suggested that cellular monitoring of mtDNA homeostasis cooperates with canonical virus sensing mechanisms to fully engage antiviral innate immunity.
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Targeting mitochondria metabolism for cancer therapy

TL;DR: Accumulating evidence now suggests that mitochondrial bioenergetics, biosynthesis and signaling are required for tumorigenesis, and emerging studies have begun to demonstrate that mitochondrial metabolism is potentially a fruitful arena for cancer therapy.
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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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The multifaceted roles of fatty acid synthesis in cancer

TL;DR: This Review explores how different aspects of FA synthesis promote tumorigenesis and tumour progression and strategies to target this pathway have not yet translated into clinical practice.
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Acetyl Coenzyme A: A Central Metabolite and Second Messenger

TL;DR: By influencing the acetylation profile of several proteins, including histones, acetyl-CoA controls key cellular processes, including energy metabolism, mitosis, and autophagy, both directly and via the epigenetic regulation of gene expression.
References
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Journal ArticleDOI

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Why do cancers have high aerobic glycolysis

TL;DR: In this article, the authors propose that persistent metabolism of glucose to lactate even in aerobic conditions is an adaptation to intermittent hypoxia in pre-malignant lesions, which leads to microenvironmental acidosis requiring evolution to phenotypes resistant to acid-induced cell toxicity.
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The biology of cancer: metabolic reprogramming fuels cell growth and proliferation

TL;DR: 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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A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

TL;DR: The mitochondria provide a direct link between the authors' environment and their genes and the mtDNA variants that permitted their forbears to energetically adapt to their ancestral homes are influencing their health today.
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Trending Questions (1)
Cancers that require more mitochondria

The provided paper does not specifically mention which types of cancers require more mitochondria.