Cancer and metabolism

2016 ◽  
pp. 119-124
Author(s):  
Cameron Snell ◽  
Kevin C. Gatter ◽  
Adrian L. Harris ◽  
Francesco Pezzella
Keyword(s):  
Tumour Growth ◽  
Glycogen Synthesis ◽  
Metabolic Reprogramming ◽  
Suppressor Activity ◽  
Metabolic Switch ◽  
Metabolic Genes ◽  
Tumour Suppressor Activity ◽  
Metabolic Transformation ◽  
The Relationship

This chapter covers the relationship between cancer and metabolism. It discusses the role of angiogenesis and metabolic reprogramming in influencing tumour growth. The transcription factors that orchestrate the metabolic switch are discussed. The chapter presents an overview of the contribution of tumour suppressors to increased glycolysis. The metabolic changes that support uncontrolled proliferation such as lactate and pH levels, hypoxia, and reactive oxygen species are discussed. The chapter also covers the contribution of metabolic genes with oncogenic or tumour suppressor activity to metabolic transformation, the upregulation of lipid biosynthesis in cancer, and glycogen synthesis in cancer. The chapter concludes with a description of the potential strategies for targeting metabolic transformation.

Cancer and metabolism

2016 ◽  
pp. 119-124
Author(s):  
Cameron Snell ◽  
Kevin C. Gatter ◽  
Adrian L. Harris ◽  
Francesco Pezzella
Keyword(s):  
Tumour Growth ◽  
Glycogen Synthesis ◽  
Metabolic Reprogramming ◽  
Suppressor Activity ◽  
Metabolic Switch ◽  
Metabolic Genes ◽  
Tumour Suppressor Activity ◽  
Metabolic Transformation ◽  
The Relationship

This chapter covers the relationship between cancer and metabolism. It discusses the role of angiogenesis and metabolic reprogramming in influencing tumour growth. The transcription factors that orchestrate the metabolic switch are discussed. The chapter presents an overview of the contribution of tumour suppressors to increased glycolysis. The metabolic changes that support uncontrolled proliferation such as lactate and pH levels, hypoxia, and reactive oxygen species are discussed. The chapter also covers the contribution of metabolic genes with oncogenic or tumour suppressor activity to metabolic transformation, the upregulation of lipid biosynthesis in cancer, and glycogen synthesis in cancer. The chapter concludes with a description of the potential strategies for targeting metabolic transformation.

scholarly journals Repression of differentiation genes by Hes transcription factors fuels neural tumour growth in Drosophila

2021 ◽  
Author(s):  
Chrysanthi Voutyraki ◽  
Alexandros Choromidis ◽  
Vasiliki Theodorou ◽  
Christina Efraimoglou ◽  
Gerasimos Anagnostopoulos ◽  
...  
Keyword(s):  
Stem Cell ◽  
Transcription Factors ◽  
Notch Signaling ◽  
Tumour Growth ◽  
Metabolic Reprogramming ◽  
Cell Physiology ◽  
Malignant Tumours ◽  
Rna Profiling ◽  
A Cell

Background: Neural stem cells (NSC) in divide asymmetrically to generate a cell that retains stem cell identity and another that is routed to differentiation. Prolonged mitotic activity of the NSCs gives rise to the plethora of neurons and glial cells that wire the brain and nerve cord. Genetic insults, such as excess of Notch signaling, perturb the normal NSC proliferation programs and trigger the formation of NSC hyperplasias, that can later progress to malignancies. Hes proteins are crucial mediators of Notch signaling and in the NSC context they act by repressing a cohort of early pro-differentiation transcription factors. Downregulation of these pro-differentiation factors makes NSC progeny cells susceptible to adopting an aberrant stem cell program. We have recently shown that Hes overexpression in Drosophila leads to NSC hyperplasias that progress to malignant tumours after allografting to adult hosts. Methods: We have combined genetic analysis, tissue allografting and transcriptomic approaches to address the role of Hes genes in NSC malignant transformation. Results: We show that the E(spl) genes are important mediators in the progression of Notch hyperplasias to malignancy, since allografts lacking the E(spl) genes grow much slower. We further present RNA profiling of Hes-induced tumours at two different stages after allografting. We find that the same cohort of differentiation-promoting transcription factors that are repressed in the primary hyperplasias continue to be downregulated after transplantation. This is accompanied by an upregulation of stress-response genes and metabolic reprogramming. Conclusions: The combination of dedifferentiation and cell physiology changes most likely drive tumour growth.

scholarly journals Advances in the role of m6A RNA modification in cancer metabolic reprogramming

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiu Han ◽  
Lin Wang ◽  
Qingzhen Han
Keyword(s):  
Cancer Cells ◽  
Epigenetic Modification ◽  
Metabolic Reprogramming ◽  
Regulatory Mechanisms ◽  
Rna Modification ◽  
Biological Functions ◽  
Rna Transcription ◽  
Cellular Processes ◽  
Metabolic Genes

Abstract N6-methyladenosine (m6A) modification is the most common internal modification of eukaryotic mRNA and is widely involved in many cellular processes, such as RNA transcription, splicing, nuclear transport, degradation, and translation. m6A has been shown to plays important roles in the initiation and progression of various cancers. The altered metabolic programming of cancer cells promotes their cell-autonomous proliferation and survival, leading to an indispensable hallmark of cancers. Accumulating evidence has demonstrated that this epigenetic modification exerts extensive effects on the cancer metabolic network by either directly regulating the expression of metabolic genes or modulating metabolism-associated signaling pathways. In this review, we summarized the regulatory mechanisms and biological functions of m6A and its role in cancer metabolic reprogramming.

scholarly journals Glucose-6 Phosphate, a Central Hub for Liver Carbohydrate Metabolism

Metabolites ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 282 ◽  
Author(s):  
Fabienne Rajas ◽  
Amandine Gautier-Stein ◽  
Gilles Mithieux
Keyword(s):  
Glucose Metabolism ◽  
Metabolic Diseases ◽  
De Novo ◽  
Glycogen Synthesis ◽  
Metabolic Reprogramming ◽  
De Novo Lipogenesis ◽  
Type I ◽  
Alcoholic Fatty Liver ◽  
Hexosamine Pathway

Cells efficiently adjust their metabolism according to the abundance of nutrients and energy. The ability to switch cellular metabolism between anabolic and catabolic processes is critical for cell growth. Glucose-6 phosphate is the first intermediate of glucose metabolism and plays a central role in the energy metabolism of the liver. It acts as a hub to metabolically connect glycolysis, the pentose phosphate pathway, glycogen synthesis, de novo lipogenesis, and the hexosamine pathway. In this review, we describe the metabolic fate of glucose-6 phosphate in a healthy liver and the metabolic reprogramming occurring in two pathologies characterized by a deregulation of glucose homeostasis, namely type 2 diabetes, which is characterized by fasting hyperglycemia; and glycogen storage disease type I, where patients develop severe hypoglycemia during short fasting periods. In these two conditions, dysfunction of glucose metabolism results in non-alcoholic fatty liver disease, which may possibly lead to the development of hepatic tumors. Moreover, we also emphasize the role of the transcription factor carbohydrate response element-binding protein (ChREBP), known to link glucose and lipid metabolisms. In this regard, comparing these two metabolic diseases is a fruitful approach to better understand the key role of glucose-6 phosphate in liver metabolism in health and disease.

scholarly journals A constitutive active allele of the transcription factor Msn2 mimicking low PKA activity dictates metabolic remodeling in yeast

2018 ◽  
Vol 29 (23) ◽  
pp. 2848-2862 ◽  
Author(s):  
Vera Pfanzagl ◽  
Wolfram Görner ◽  
Martin Radolf ◽  
Alexandra Parich ◽  
Rainer Schuhmacher ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Signature ◽  
Metabolic Reprogramming ◽  
Diauxic Shift ◽  
Environmental Stress Response ◽  
Metabolic Switch ◽  
Metabolic Remodeling ◽  
Active Allele ◽  
Limited Degree

In yeast, protein kinase A (PKA) adjusts transcriptional profiles, metabolic rates, and cell growth in accord with carbon source availability. PKA affects gene expression mostly via the transcription factors Msn2 and Msn4, two key regulators of the environmental stress response. Here we analyze the role of the PKA-Msn2 signaling module using an Msn2 allele that harbors serine-to-alanine substitutions at six functionally important PKA motifs (Msn2A6) . Expression of Msn2A6 mimics low PKA activity, entails a transcription profile similar to that of respiring cells, and prevents formation of colonies on glucose-containing medium. Furthermore, Msn2A6 leads to high oxygen consumption and hence high respiratory activity. Substantially increased intracellular concentrations of several carbon metabolites, such as trehalose, point to a metabolic adjustment similar to diauxic shift. This partial metabolic switch is the likely cause for the slow-growth phenotype in the presence of glucose. Consistently, Msn2A6 expression does not interfere with growth on ethanol and tolerated is to a limited degree in deletion mutant strains with a gene expression signature corresponding to nonfermentative growth. We propose that the lethality observed in mutants with hampered PKA activity resides in metabolic reprogramming that is initiated by Msn2 hyperactivity.

scholarly journals Interplay of Immunometabolism and Epithelial–Mesenchymal Transition in the Tumor Microenvironment

2021 ◽  
Vol 22 (18) ◽  
pp. 9878
Author(s):  
Ming-Yu Chou ◽  
Muh-Hwa Yang
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Immune Surveillance ◽  
Metabolic Reprogramming ◽  
Mesenchymal Transition ◽  
Regulatory Loop ◽  
The Relationship

Epithelial–mesenchymal transition (EMT) and metabolic reprogramming in cancer cells are the key hallmarks of tumor metastasis. Since the relationship between the two has been well studied, researchers have gained increasing interest in the interplay of cancer cell EMT and immune metabolic changes. Whether the mutual influences between them could provide novel explanations for immune surveillance during metastasis is worth understanding. Here, we review the role of immunometabolism in the regulatory loop between tumor-infiltrating immune cells and EMT. We also discuss the challenges and perspectives of targeting immunometabolism in cancer treatment.

scholarly journals Metabolic Reprogramming and Renal Fibrosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiaoyu Zhu ◽  
Lili Jiang ◽  
Mengtuan Long ◽  
Xuejiao Wei ◽  
Yue Hou ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Potential Role ◽  
Acid Metabolism ◽  
Metabolic Reprogramming ◽  
Novel Drugs ◽  
Future Challenges ◽  
And Function ◽  
Relationship Of ◽  
The Relationship

There are several causes of chronic kidney disease, but all of these patients have renal fibrosis. Although many studies have examined the pathogenesis of renal fibrosis, there are still no effective treatments. A healthy and balanced metabolism is necessary for normal cell growth, proliferation, and function, but metabolic abnormalities can lead to pathological changes. Normal energy metabolism is particularly important for maintaining the structure and function of the kidneys because they consume large amounts of energy. We describe the metabolic reprogramming that occurs during renal fibrosis, which includes changes in fatty acid metabolism and glucose metabolism, and the relationship of these changes with renal fibrosis. We also describe the potential role of novel drugs that disrupt this metabolic reprogramming and the development of fibrosis, and current and future challenges in the treatment of fibrosis.

scholarly journals The Role of MicroRNAs in Lung Cancer Metabolism

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1716
Author(s):  
Mohamed Iman Hidayat Nor Azizi ◽  
Iekhsan Othman ◽  
Rakesh Naidu
Keyword(s):  
Lung Cancer ◽  
Differential Expression ◽  
Cancer Metabolism ◽  
Mirna Expression Profile ◽  
Metabolic Reprogramming ◽  
Lung Cancers ◽  
Post Transcriptional Regulation ◽  
The Relationship ◽  
Insight Into

MicroRNAs (miRNAs) are short-strand non-coding RNAs that are responsible for post-transcriptional regulation of many biological processes. Their differential expression is important in supporting tumorigenesis by causing dysregulation in normal biological functions including cell proliferation, apoptosis, metastasis and invasion and cellular metabolism. Cellular metabolic processes are a tightly regulated mechanism. However, cancer cells have adapted features to circumvent these regulations, recognizing metabolic reprogramming as an important hallmark of cancer. The miRNA expression profile may differ between localized lung cancers, advanced lung cancers and solid tumors, which lead to a varying extent of metabolic deregulation. Emerging evidence has shown the relationship between the differential expression of miRNAs with lung cancer metabolic reprogramming in perpetuating tumorigenesis. This review provides an insight into the role of different miRNAs in lung cancer metabolic reprogramming by targeting key enzymes, transporter proteins or regulatory components alongside metabolic signaling pathways. These discussions would allow a deeper understanding of the importance of miRNAs in tumor progression therefore providing new avenues for diagnostic, therapeutic and disease management applications.

scholarly journals The role of S-nitrosylation of PFKM in regulation of glycolysis in ovarian cancer cells

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Wenwen Gao ◽  
Mengqiu Huang ◽  
Xi Chen ◽  
Jianping Chen ◽  
Zhiwei Zou ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Nitrogen Oxide ◽  
Cancer Cells ◽  
Critical Role ◽  
Xenograft Model ◽  
Metabolic Reprogramming ◽  
Ovarian Cancer Cells ◽  
Metabolic Switch ◽  
Mouse Xenograft Model

AbstractOne of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancer cells, and reduced tumor growth and metastasis in the mouse xenograft model. These findings indicated that S-nitrosylation at Cys351 of PFKM by NOS1 contributes to the metabolic reprogramming of ovarian cancer cells, highlighting a critical role of endogenous nitrogen oxide on metabolism regulations in tumor progression.

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