Metabolic Reprogramming, Questioning, and Implications for Cancer

Jacquet, Pierre; Stéphanou, Angélique

doi:10.3390/biology10020129

Cited by 13 publications

(11 citation statements)

References 39 publications

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“…These can include increased inflammation, anti-apoptosis, immune evasion, and the production and accumulation of advanced glycation end products (AGEs) [ 226 ]. Some of these effects are essential for viral replication and promotion of tumors, while others are byproducts of the changes that occur with metabolic reprogramming and help modify the cellular environment ( Figure 4 ) [ 227 ].…”

Section: Non-metabolic Effects Of Metabolic Reprogrammingmentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to metabolic reprogramming, seven main hallmarks can be identified: (1) increased glycolysis and lactic acid, (2) increased glutaminolysis, (3) increased pentose phosphate pathway, (4) mitochondrial changes, (5) increased lipid metabolism, (6) changes in amino acid metabolism, and (7) changes in other biosynthetic and bioenergetic pathways. Viruses depend on metabolic reprogramming to increase biomass to fuel viral genome replication and production of new virions. Viruses take advantage of the non-metabolic effects of metabolic reprogramming, creating an anti-apoptotic environment and evading the immune system. Other non-metabolic effects can negatively affect cellular function. Understanding the role metabolic reprogramming plays in viral pathogenesis may provide better therapeutic targets for antivirals.

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Section: Non-metabolic Effects Of Metabolic Reprogrammingmentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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“…The two states “glycolysis” and “OXPHOS”, do not really fully exclude one another (except in cases of anoxia or saturation of downstream metabolites), since pyruvate produced through glycolysis is needed to fuel TCA-OXPHOS. With respect to reprogramming, we dedicated a paper to this issue [ 69 ], highlighting the fact that this term implied genetic mutations which were not necessarily required. Rather than “reprogramming”, the term “adaptability” is more appropriate to describe the true evolution of the metabolic cell state.…”

Section: Discussionmentioning

confidence: 99%

“…The expression “metabolic switch” began to be progressively replaced by the more permissive expression “metabolic reprogramming” in the interpretation of a change in metabolic phenotype ( Figure 5 ). We previously dedicated a whole paper to this subject [ 69 ].…”

Section: Differences Around the Concepts Associated With The Warburg ...mentioning

confidence: 99%

Searching for the Metabolic Signature of Cancer: A Review from Warburg’s Time to Now

Jacquet

Stéphanou

2022

Biomolecules

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This review focuses on the evolving understanding that we have of tumor cell metabolism, particularly glycolytic and oxidative metabolism, and traces back its evolution through time. This understandng has developed since the pioneering work of Otto Warburg, but the understanding of tumor cell metabolism continues to be hampered by misinterpretation of his work. This has contributed to the use of the new concepts of metabolic switch and metabolic reprogramming, that are out of step with reality. The Warburg effect is often considered to be a hallmark of cancer, but is it really? More generally, is there a metabolic signature of cancer? We draw the conclusion that the signature of cancer cannot be reduced to a single factor, but is expressed at the tissue level in terms of the capacity of cells to dynamically explore a vast metabolic landscape in the context of significant environmental heterogeneities.

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“…Establishing a temporal hierarchy of these metabolic adaptations is challenging. However, metabolic pathways interact with each other, and all of them have the potential to become the ultimate trigger for cancer [32]. Thus, it is as important to identify whether these metabolic adaptations are reversible, as it is to identify temporal hierarchy.…”

Section: Dmentioning

confidence: 99%

Heterogeneity of metabolic adaptive capacity affects the prognosis among pancreatic ductal adenocarcinomas

et al. 2022

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Background Evolutionary cancer has a supply mechanism to satisfy higher energy demands even in poor-nutrient conditions. Metabolic reprogramming is essential to supply sufficient energy. The relationship between metabolic reprogramming and the clinical course of pancreatic ductal adenocarcinoma (PDAC) remains unclear. We aimed to clarify the differences in metabolic status among PDAC patients. Methods We collected clinical data from 128 cases of resectable PDAC patients undergoing surgery. Sixty-three resected tissues, 15 tissues from the low carbohydrate antigen 19-9 (CA19-9), 38–100 U/mL, and high CA19-9, > 500 U/mL groups, and 33 non-tumor control parts, were subjected to tandem mass spectrometry workflow to systematically explore metabolic status. Clinical and proteomic data were compared on the most used PDAC biomarker, preoperative CA19-9 value. Results Higher CA19-9 levels were clearly associated with higher early recurrence (p < 0.001), decreased RFS (p < 0.001), and decreased DSS (p = 0.025). From proteomic analysis, we discovered that cancer evolution-related as well as various metabolism-related pathways were more notable in the high group. Using resected tissue immunohistochemical staining, we learned that high CA19-9 PDAC demonstrated aerobic glycolysis enhancement, yet no decrease in protein synthesis. We found a heterogeneity of various metabolic processes, including carbohydrates, proteins, amino acids, lipids, and nucleic acids, between the low and the high groups, suggesting differences in metabolic adaptive capacity. Conclusions Our study found metabolic adaptation differences among PDAC cases, pertaining to both cancer evolution and the prognosis. CA19-9 can help estimate the metabolic adaptive capacity of energy supply for PDAC evolution.

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Metabolic Reprogramming, Questioning, and Implications for Cancer

Cited by 13 publications

References 39 publications

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Searching for the Metabolic Signature of Cancer: A Review from Warburg’s Time to Now

Heterogeneity of metabolic adaptive capacity affects the prognosis among pancreatic ductal adenocarcinomas

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