Gluconeogenesis in cancer cells - Repurposing of a starvation-induced metabolic pathway?
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TLDR
Light is shed on the current knowledge of cancer cell gluconeogenesis and its role in metabolic reprogramming, cancer cell plasticity, and tumor growth and fructose-1,6-bisphosphatase 1, a downstream gluc oneogenesis enzyme, inhibits glycolysis and tumorgrowth.About:
This article is published in Biochimica et Biophysica Acta.The article was published on 2019-08-01 and is currently open access. It has received 126 citations till now. The article focuses on the topics: Metabolic pathway & Phosphoenolpyruvate carboxykinase.read more
Citations
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Journal ArticleDOI
Distribution and prognostic significance of gluconeogenesis and glycolysis in lung cancer.
Elisabeth Smolle,Petra Leko,Elvira Stacher-Priehse,Luka Brcic,Amin El-Heliebi,Lilli Hofmann,Franz Quehenberger,Andelko Hrzenjak,Helmut Popper,Horst Olschewski,Katharina Leithner +10 more
TL;DR: The results of this study show that glycolysis and gluconeogenesis are activated in NSCLC in a tumor size and oxygenation modulated manner and differentially correlate with outcome.
Journal ArticleDOI
Gluconeogenic enzyme PCK1 deficiency promotes CHK2 O-GlcNAcylation and hepatocellular carcinoma growth upon glucose deprivation
Jin Xiang,Chang Chen,Rui Liu,Dongmei Gou,Lei Chang,Haijun Deng,Qingzhu Gao,Wanjun Zhang,Lin Tuo,Xuanming Pan,Li Liang,Jie Xia,Lu-Yi Huang,Ke Yao,Bohong Wang,Zeping Hu,Ailong Huang,Kai Wang,Ni Tang +18 more
TL;DR: In this paper, the gluconeogenic enzyme phosphoenolpyruvate carboxykinase 1 (PCK1) is downregulated in hepatocellular carcinoma (HCC) and showed a link between PCK1 depletion and hyper-O-GlcNAcylation that underlies HCC oncogenesis.
Journal ArticleDOI
The Metabolic Fates of Pyruvate in Normal and Neoplastic Cells.
Edward V. Prochownik,Huabo Wang +1 more
TL;DR: In this paper, the authors discuss the six pathways that influence pyruvate content and utilization: 1. The lactate dehydrogenase pathway that either converts excess pyruVate to lactate or regenerates pyVate from lactate for use as a fuel or biosynthetic substrate.
Journal ArticleDOI
Cysteine as a Carbon Source, a Hot Spot in Cancer Cells Survival.
TL;DR: In the present review, emphasis will be given to the role of cysteine as a carbon source, focusing on the metabolic reliance on Cysteine, benefiting the metabolic fitness and survival of cancer cells.
Journal ArticleDOI
Amino acid metabolism as a therapeutic target in cancer: a review
TL;DR: In this article, the authors summarise these treatment strategies into three promising avenues: amino acid restriction, enzymatic depletion and inhibition of metabolism, and highlight these three current research avenues that have support in both preclinical and clinical settings.
References
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Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction
David R. Wise,Ralph J. DeBerardinis,Anthony A. Mancuso,Nabil Sayed,Xiao-yong Zhang,Harla K. Pfeiffer,Ilana Nissim,Evgueni Daikhin,Marc Yudkoff,Steven B. McMahon,Craig B. Thompson +10 more
TL;DR: It is reported that the transcriptional regulatory properties of the oncogene Myc coordinate the expression of genes necessary for cells to engage in glutamine catabolism that exceeds the cellular requirement for protein and nucleotide biosynthesis, resulting in the reprogramming of mitochondrial metabolism to depend on glutaminolysis to sustain cellular viability and TCA cycle anapleurosis.
Journal ArticleDOI
Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth
Kristin M Nieman,Hilary A. Kenny,Carla Penicka,Andras Ladanyi,Rebecca Buell-Gutbrod,Marion Zillhardt,Iris L. Romero,Mark S. Carey,Gordon B. Mills,Gökhan S. Hotamisligil,S. Diane Yamada,Marcus E. Peter,Katja Gwin,Ernst Lengyel +13 more
TL;DR: It is shown that primary human omental adipocytes promote homing, migration and invasion of ovarian cancer cells, and that adipokines including interleukin-8 (IL-8) mediate these activities, and adipocytes provide fatty acids for rapid tumor growth.
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