scholarly journals TIGAR's promiscuity

2014 ◽  
Vol 458 (3) ◽  
pp. e5-e7 ◽  
Author(s):  
Juan P. Bolaños
Keyword(s):  
Cell Metabolism ◽  
Glucose Consumption ◽  
Pentose Phosphate ◽  
Regulator Protein ◽  
Biochemical Journal ◽  
Cellular Context ◽  
Health And Disease ◽  
Rigorous Study ◽  
Cancer Cell Metabolism

TIGAR [TP53 (tumour protein 53)-induced glycolysis and apoptosis regulator] protein is known for its ability to inhibit glycolysis, shifting glucose consumption towards the pentose phosphate pathway to promote antioxidant protection of cancer cells. According to sequence homology and activity analyses, TIGAR was initially considered to be a fructose-2,6-bisphosphatase; it has thus received much attention in cancer cell metabolism, given its dependence on p53 and the key role of F26BP (fructose 2,6-bisphosphate) at modulating glycolysis and gluconeogenesis. However, in a rigorous study published in this issue of the Biochemical Journal, Gerin and colleagues report that recombinant TIGAR is a 23BPG (2,3-bisphosphoglycerate) phosphatase, although it also dephosphorylates other carboxylic acid-phosphate esters and, weakly, F26BP. As such, inhibition of endogenous TIGAR leads to a dramatic increase in cellular 23BPG, influencing F26BP to a lower extent that depends on the cellular context. These results challenge the currently held notion that TIGAR modulates glycolysis through decreasing F26BP, and opens a yet unrecognized function(s) for TIGAR-mediated 23BPG control of cellular metabolism in health and disease.

scholarly journals The Role of Cell Metabolism in Innate Immune Memory

2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea
Keyword(s):  
Metabolic Pathways ◽  
Tricarboxylic Acid Cycle ◽  
Cell Metabolism ◽  
Innate Immune ◽  
Immune Memory ◽  
Functional Changes ◽  
Trained Immunity ◽  
Health And Disease

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.

scholarly journals Glutamine-Derived Aspartate Biosynthesis in Cancer Cells: Role of Mitochondrial Transporters and New Therapeutic Perspectives

Cancers ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 245
Author(s):  
Ruggiero Gorgoglione ◽  
Valeria Impedovo ◽  
Christopher L. Riley ◽  
Deborah Fratantonio ◽  
Stefano Tiziani ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Cell Metabolism ◽  
Redox Homeostasis ◽  
Nucleotide Biosynthesis ◽  
Specific Tumor ◽  
Mitochondrial Carrier Family ◽  
Cancer Types ◽  
Cancer Cell Metabolism ◽  
Tumor Types

Aspartate has a central role in cancer cell metabolism. Aspartate cytosolic availability is crucial for protein and nucleotide biosynthesis as well as for redox homeostasis. Since tumor cells display poor aspartate uptake from the external environment, most of the cellular pool of aspartate derives from mitochondrial catabolism of glutamine. At least four transporters are involved in this metabolic pathway: the glutamine (SLC1A5_var), the aspartate/glutamate (AGC), the aspartate/phosphate (uncoupling protein 2, UCP2), and the glutamate (GC) carriers, the last three belonging to the mitochondrial carrier family (MCF). The loss of one of these transporters causes a paucity of cytosolic aspartate and an arrest of cell proliferation in many different cancer types. The aim of this review is to clarify why different cancers have varying dependencies on metabolite transporters to support cytosolic glutamine-derived aspartate availability. Dissecting the precise metabolic routes that glutamine undergoes in specific tumor types is of upmost importance as it promises to unveil the best metabolic target for therapeutic intervention.

Cancer Cell Metabolism Featuring Nrf2

2020 ◽  
Vol 17 (3) ◽  
pp. 263-271 ◽  
Author(s):  
Payal Chatterjee ◽  
Mukesh Yadav ◽  
Namrata Chauhan ◽  
Ying Huang ◽  
Yun Luo
Keyword(s):  
Cancer Cells ◽  
Cell Metabolism ◽  
Cellular Metabolism ◽  
Energy Requirements ◽  
Genetic Mutations ◽  
Cellular Protection ◽  
Key Factor ◽  
Cancer Cell Metabolism ◽  
Cancerous Cells

Although the major role of Nrf2 has long been established as a transcription factor for providing cellular protection against oxidative stress, multiple pieces of research and reviews now claim exactly the opposite. The dilemma - “to activate or inhibit” the protein requires an immediate answer, which evidently links cellular metabolism to the causes and purpose of cancer. Profusely growing cancerous cells have prolific energy requirements, which can only be fulfilled by modulating cellular metabolism. This review highlights the cause and effect of Nrf2 modulation in cancer that in turn channelize cellular metabolism, thereby fulfilling the energy requirements of cancer cells. The present work also highlights the purpose of genetic mutations in Nrf2, in relation to cellular metabolism in cancer cells, thus pointing out a newer approach where parallel mutations may be the key factor to decide whether to activate or inhibit Nrf2.

RED CELL METABOLISM IN THE PREMATURE INFANT

PEDIATRICS ◽  
1967 ◽  
Vol 39 (5) ◽  
pp. 689-695
Author(s):  
Frank A. Oski
Keyword(s):  
Premature Infants ◽  
Pentose Phosphate Pathway ◽  
Cell Metabolism ◽  
Glucose Consumption ◽  
Pentose Phosphate ◽  
Red Cells ◽  
Red Cell ◽  
O2 Production ◽  
Cell Glucose ◽  
Normal Adults

Red cell glucose consumption and C14 O2 production from glucose-I-C14 and glucose-U-C14 were measured in 17 premature infants, 15 normal adults and 7 patients with reticulocytosis. The red cells from the premature infants consumed significantly more glucose and produced more C14 O2 than did the cells from normal adults but did not differ in this regard from patients with elevated reticulocyte counts. The percent of glucose metabolized by the pentose phosphate pathway in the red cells of the infants was as great, and often greater, than that observed in the other two groups. The red cells of the premature infants also demonstrated an ability to respond to methylene blue. The pentose phosphate pathway would appear to be intact in the red cells from these infants and inadequate generation of NADPH2 is not responsible for the ease with which these cells develop oxidative denaturation of hemoglobin.

scholarly journals Cancer cell metabolism: the essential role of the nonessential amino acid, glutamine

2017 ◽  
Vol 36 (10) ◽  
pp. 1302-1315 ◽  
Author(s):  
Ji Zhang ◽  
Natalya N Pavlova ◽  
Craig B Thompson
Keyword(s):  
Amino Acid ◽  
Cancer Cell ◽  
Essential Role ◽  
Cell Metabolism ◽  
Nonessential Amino Acid ◽  
Cancer Cell Metabolism

scholarly journals WNT Signaling: an Emerging Mediator of Cancer Cell Metabolism?

2014 ◽  
Vol 35 (1) ◽  
pp. 2-10 ◽  
Author(s):  
Victoria Sherwood
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathways ◽  
Cancer Cell ◽  
Cancer Metabolism ◽  
Cell Metabolism ◽  
Critical Role ◽  
Oncogenic Signaling ◽  
Cancer Cell Metabolism ◽  
Oncogenic Signaling Pathways

WNT signaling was discovered in tumor models and has been recognized as a regulator of cancer development and progression for over 3 decades. Recent work has highlighted a critical role for WNT signaling in the metabolic homeostasis of mammals, where its misregulation has been heavily implicated in diabetes. While the majority of WNT metabolism research has focused on nontransformed tissues, the role of WNT in cancer metabolism remains underinvestigated. Cancer is also a metabolic disease where oncogenic signaling pathways regulate energy production and macromolecular synthesis to fuel rapidly proliferating tumors. This review highlights the emerging evidence for WNT signaling in the reprogramming of cancer cell metabolism and examines the role of these signaling pathways as mediators of tumor bioenergetics.

scholarly journals The VHL/HIF Axis in the Development and Treatment of Pheochromocytoma/Paraganglioma

2020 ◽  
Vol 11 ◽  
Author(s):  
Song Peng ◽  
Jun Zhang ◽  
Xintao Tan ◽  
Yiqiang Huang ◽  
Jing Xu ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Metabolic Diseases ◽  
Cell Metabolism ◽  
Germline Mutations ◽  
Genetic Alterations ◽  
The Road ◽  
Cancer Cell Metabolism ◽  
Underlying Mechanisms ◽  
Lines Of Evidence

Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors originating from chromaffin cells in the adrenal medulla (PCCs) or extra-adrenal sympathetic or parasympathetic paraganglia (PGLs). About 40% of PPGLs result from germline mutations and therefore they are highly inheritable. Although dysfunction of any one of a panel of more than 20 genes can lead to PPGLs, mutations in genes involved in the VHL/HIF axis including PHD, VHL, HIF-2A (EPAS1), and SDHx are more frequently found in PPGLs. Multiple lines of evidence indicate that pseudohypoxia plays a crucial role in the tumorigenesis of PPGLs, and therefore PPGLs are also known as metabolic diseases. However, the interplay between VHL/HIF-mediated pseudohypoxia and metabolic disorder in PPGLs cells is not well-defined. In this review, we will first discuss the VHL/HIF axis and genetic alterations in this axis. Then, we will dissect the underlying mechanisms in VHL/HIF axis-driven PPGL pathogenesis, with special attention paid to the interplay between the VHL/HIF axis and cancer cell metabolism. Finally, we will summarize the currently available compounds/drugs targeting this axis which could be potentially used as PPGLs treatment, as well as their underlying pharmacological mechanisms. The overall goal of this review is to better understand the role of VHL/HIF axis in PPGLs development, to establish more accurate tools in PPGLs diagnosis, and to pave the road toward efficacious therapeutics against metastatic PPGLs.

scholarly journals Role of tyrosine phosphorylation in modulating cancer cell metabolism

2020 ◽  
Vol 1874 (2) ◽  
pp. 188442
Author(s):  
Maria Letizia Taddei ◽  
Elisa Pardella ◽  
Erica Pranzini ◽  
Giovanni Raugei ◽  
Paolo Paoli
Keyword(s):  
Tyrosine Phosphorylation ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Cancer Cell Metabolism
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