Dysregulated metabolic enzymes and metabolicï¿½reprogramming in cancer cells (Review)

Sreedhar, Annapoorna; Zhao, Yunfeng

doi:10.3892/br.2017.1022

Cited by 50 publications

(53 citation statements)

References 102 publications

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“…Overall, macromolecule biosynthesis and mitochondrial biogenesis, as well as cellular redox homeostasis, are perturbed (DeBerardinis & Chandel, 2016;Liu et al, 2019;Orang, Petersen, McKinnon, & Michael, 2019;Phan, Yeung, & Lee, 2014). Indeed, the process of tumorigenesis and mitochondrial biology interplays at multiple levels, ranging from direct oncogenic signaling from mitochondria to perturbation of mitochondrial functions, often caused by mutation in mitochondrial proteins (Sreedhar & Zhao, 2018).…”

Section: Introductionmentioning

confidence: 99%

Characterization of human frataxin missense variants in cancer tissues

et al. 2019

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Human frataxin is an iron‐binding protein involved in the mitochondrial iron–sulfur (Fe–S) clusters assembly, a process fundamental for the functional activity of mitochondrial proteins. Decreased level of frataxin expression is associated with the neurodegenerative disease Friedreich ataxia. Defective function of frataxin may cause defects in mitochondria, leading to increased tumorigenesis. Tumor‐initiating cells show higher iron uptake, a decrease in iron storage and a reduced Fe–S clusters synthesis and utilization. In this study, we selected, from COSMIC database, the somatic human frataxin missense variants found in cancer tissues p.D104G, p.A107V, p.F109L, p.Y123S, p.S161I, p.W173C, p.S181F, and p.S202F to analyze the effect of the single amino acid substitutions on frataxin structure, function, and stability. The spectral properties, the thermodynamic and the kinetic stability, as well as the molecular dynamics of the frataxin missense variants found in cancer tissues point to local changes confined to the environment of the mutated residues. The global fold of the variants is not altered by the amino acid substitutions; however, some of the variants show a decreased stability and a decreased functional activity in comparison with that of the wild‐type protein.

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Section: Introductionmentioning

confidence: 99%

Characterization of human frataxin missense variants in cancer tissues

et al. 2019

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“…Glycolysis is an oxygen‐independent metabolic pathway that converts glucose into pyruvate through a 10‐step biochemical reaction to produce adenosine triphosphate (ATP). The three main enzymatic reactions responsible for the control of glycolytic flux are catalysed by hexokinase, phosphofructokinase and pyruvate kinase . Under aerobic conditions, pyruvate is commonly transported into mitochondria and converted to acetyl‐CoA.…”

Section: Metabolic Pathways Implicated In Cldmentioning

confidence: 99%

“…Acetyl‐CoA, which is derived via beta‐oxidation, enters the TCA cycle to produce nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH2), the electron carriers that donate electrons to the electron transport chain. This subsequently leads to ATP generation . Regulation of the TCA cycle is heavily dependent on the availability of enzyme substrates.…”

Section: Metabolic Pathways Implicated In Cldmentioning

confidence: 99%

Metabolomics in chronic lung diseases

et al. 2019

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Chronic lung diseases represent a significant global burden. Their increasing incidence and complexity render a comprehensive, multidisciplinary and personalized approach to each patient, critically important. Most recently, unique biochemical pathways and disease markers have been identified through large‐scale metabolomic studies. Metabolomics is the study of metabolic pathways and the measurement of unique biomolecules in a living system. Analysing samples from different compartments such as bronchoalveolar lavage fluid (BALF) and plasma has proven useful for the characterization of a number of pathological conditions and offers promise as a clinical tool. For example, several studies using mass spectrometry (MS) have shown alterations in the sphingolipid metabolism of chronic obstructive pulmonary disease (COPD) sufferers. In this article, we present a practical review of the application of metabolomics to the study of chronic lung diseases (CLD): COPD, idiopathic pulmonary fibrosis (IPF) and asthma. The insights, which the analytical strategies employed in metabolomics, have provided to the dissection of the biochemistry of CLD and future clinical biomarkers are explored.

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“…Metabolic enzymes carry out a wide range of catalytic activities and are responsible for a variety of cellular functions necessary for cancer survival. A growing body of evidence indicates that metabolic enzymes possess both metabolic and nonmetabolic activities that are critical in the development of NSCLC …”

mentioning

confidence: 99%

Functions of metabolic enzymes in the development of non‐small cell lung cancer

Zhao

2019

Thoracic Cancer

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Dysregulated metabolic enzymes and metabolicï¿½reprogramming in cancer cells (Review)

Cited by 50 publications

References 102 publications

Characterization of human frataxin missense variants in cancer tissues

Characterization of human frataxin missense variants in cancer tissues

Metabolomics in chronic lung diseases

Functions of metabolic enzymes in the development of non‐small cell lung cancer

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