Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA
An S. Tan,James W. Baty,Lan-Feng Dong,Ayenachew Bezawork-Geleta,Berwini Endaya,Jacob Goodwin,Martina Bajzikova,Jaromira Kovarova,Martin Peterka,Bing Yan,Elham Alizadeh Pesdar,Margarita Sobol,Anatolyj Filimonenko,Shani Stuart,Magdalena Vondrusova,Katarina Kluckova,Karishma Sachaphibulkij,Jakub Rohlena,Pavel Hozák,Jaroslav Truksa,David Eccles,Larisa M. Haupt,Lyn R. Griffiths,Jiri Neuzil,Jiri Neuzil,Michael V. Berridge +25 more
TLDR
This paper showed that tumor cells without mitochondrial DNA (mtDNA) showed delayed tumor growth, and that tumor formation is associated with acquisition of mtDNA from host cells, leading to partial recovery of mitochondrial function in cells derived from primary tumors grown from cells without mtDNA and a shorter lag in tumor growth.About:
This article is published in Cell Metabolism.The article was published on 2015-01-06 and is currently open access. It has received 548 citations till now. The article focuses on the topics: Respiratory function & Tumor microenvironment.read more
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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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Cancer metabolism: a therapeutic perspective
Ubaldo E. Martinez-Outschoorn,Maria Peiris-Pagès,Richard G. Pestell,Federica Sotgia,Federica Sotgia,Michael P. Lisanti +5 more
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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Supporting Aspartate Biosynthesis Is an Essential Function of Respiration in Proliferating Cells
Lucas B. Sullivan,Dan Y. Gui,Aaron M. Hosios,Lauren N. Bush,Elizaveta Freinkman,Matthew G. Vander Heiden,Matthew G. Vander Heiden +6 more
TL;DR: It is found that electron acceptors are limiting for producing aspartates, and supplying aspartate enables proliferation of respiration deficient cells in the absence of exogenous electron acceptor.
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Mitochondrial metabolism and cancer.
Paolo E. Porporato,Nicoletta Filigheddu,José Manuel Bravo-San Pedro,Guido Kroemer,Lorenzo Galluzzi,Lorenzo Galluzzi +5 more
TL;DR: The cancer cell-intrinsic and cell-extrinsics mechanisms through which mitochondria influence all steps of oncogenesis are reviewed, with a focus on the therapeutic potential of targeting mitochondrial metabolism for cancer therapy.
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Mitochondria and Cancer
TL;DR: Mitochondria play a central and multifunctional role in malignant tumor progression, and targeting mitochondria provides therapeutic opportunities.
References
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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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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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Mutational landscape and significance across 12 major cancer types
Cyriac Kandoth,Michael D. McLellan,Fabio Vandin,Kai Ye,Beifang Niu,Charles Lu,Mingchao Xie,Qunyuan Zhang,Joshua F. McMichael,Matthew A. Wyczalkowski,Mark D.M. Leiserson,Christopher A. Miller,John S. Welch,Matthew J. Walter,Michael C. Wendl,Timothy J. Ley,Richard K. Wilson,Benjamin J. Raphael,Li Ding +18 more
TL;DR: Data and analytical results for point mutations and small insertions/deletions from 3,281 tumours across 12 tumour types are presented as part of the TCGA Pan-Cancer effort, and clinical association analysis identifies genes having a significant effect on survival.
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Beyond aerobic glycolysis : Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis
Ralph J. DeBerardinis,Anthony A. Mancuso,Evgueni Daikhin,Ilana Nissim,Marc Yudkoff,Suzanne Wehrli,Craig B. Thompson +6 more
TL;DR: Transformed cells exhibit a high rate of glutamine consumption that cannot be explained by the nitrogen demand imposed by nucleotide synthesis or maintenance of nonessential amino acid pools, and glutamine metabolism provides a carbon source that facilitates the cell's ability to use glucose-derived carbon and TCA cycle intermediates as biosynthetic precursors.
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Tumor Cell Metabolism: Cancer's Achilles' Heel
TL;DR: The peculiarities of tumor cell metabolism are reviewed to discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.