The rate of glycolysis quantitatively mediates specific histone acetylation sites
Conclusions
We demonstrate that histone acylation is directly sensed by glucose flux in a titratable, dose-dependent manner that is modulated by glycolytic flux and that a possible function of the Warburg Effect, a metabolic state observed in cancers with enhanced glucose metabolism, is to confer specific signaling effects on cells. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - September 23, 2015 Category: Cancer & Oncology Source Type: research
The rate of glycolysis quantitatively mediates specific histone acetylation sites
Conclusions < /h3 > < p class= " a-plus-plus " > We demonstrate that histone acylation is directly sensed by glucose flux in a titratable, dose-dependent manner that is modulated by glycolytic flux and that a possible function of the Warburg Effect, a metabolic state observed in cancers with enhanced glucose metabolism, is to confer specific signaling effects on cells. < /p > < /span > (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - September 22, 2015 Category: Cancer & Oncology Source Type: research
13 C-labeled biochemical probes for the study of cancer metabolism with dynamic nuclear polarization-enhanced magnetic resonance imaging
Abstract
In recent years, advances in metabolic imaging have become dependable tools for the diagnosis and treatment assessment in cancer. Dynamic nuclear polarization (DNP) has recently emerged as a promising technology in hyperpolarized (HP) magnetic resonance imaging (MRI) and has reached clinical relevance with the successful visualization of [1-13C] pyruvate as a molecular imaging probe in human prostate cancer. This review focuses on introducing representative compounds relevant to metabolism that are characteristic of cancer tissue: aerobic glycolysis and pyruvate metabolism, glutamine addiction ...
Source: Cancer and Metabolism - September 14, 2015 Category: Cancer & Oncology Source Type: research
Knockout of Vdac1 activates hypoxia-inducible factor through reactive oxygen species generation and induces tumor growth by promoting metabolic reprogramming and inflammation
Conclusions
Metabolic reprogramming in cancer cells may be regulated by VDAC1 through vascular destabilization and inflammation. These findings provide new perspectives into the understanding of VDAC1 in the function of mitochondria not only in cancer but also in inflammatory diseases. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - August 26, 2015 Category: Cancer & Oncology Source Type: research
Metabolic plasticity maintains proliferation in pyruvate dehydrogenase deficient cells
Conclusions
Although PDH suppression substantially alters central carbon metabolism, the data indicate that rapid cell proliferation occurs independently of PDH activity. Our findings reveal that this central enzyme is essentially dispensable for growth and proliferation of both primary cells and established cell lines. We also identify the compensatory mechanisms that are activated under PDH deficiency, namely scavenging of extracellular lipids and lipogenic acetyl-CoA production from reductive glutamine metabolism through IDH1. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - June 29, 2015 Category: Cancer & Oncology Source Type: research
Quantification of folate metabolism using transient metabolic flux analysis
Conclusions
This work validates tMFA as a cost-effective methodology to investigate cell metabolism. Using tMFA, we have shown that the effects of treatment with the antifolate methotrexate extend beyond inhibition of purine synthesis and propagate to other pathways in central metabolism. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - May 28, 2015 Category: Cancer & Oncology Source Type: research
An epitope tag alters phosphoglycerate dehydrogenase structure and impairs ability to support cell proliferation
Conclusions
Purification of untagged recombinant PHGDH eliminates the need to use an epitope tag for enzyme studies. Furthermore, while tagged PHGDH retains some ability to convert 3PG to PHP, the structural alterations caused by including an epitope tag disrupts the ability of PHGDH to sustain cancer cell proliferation. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - April 29, 2015 Category: Cancer & Oncology Source Type: research
Mitophagy and cancer
Abstract
Mitophagy is a selective form of macro-autophagy in which mitochondria are selectively targeted for degradation in autophagolysosomes. Mitophagy can have the beneficial effect of eliminating old and/or damaged mitochondria, thus maintaining the integrity of the mitochondrial pool. However, mitophagy is not only limited to the turnover of dysfunctional mitochondria but also promotes reduction of overall mitochondrial mass in response to certain stresses, such as hypoxia and nutrient starvation. This prevents generation of reactive oxygen species and conserves valuable nutrients (such as oxygen) ...
Source: Cancer and Metabolism - March 26, 2015 Category: Cancer & Oncology Source Type: research
Treatment of glioma patients with ketogenic diets: report of two cases treated with an IRB-approved energy-restricted ketogenic diet protocol and review of the literature
Conclusions
We conclude that 1. KD is safe and without major side effects; 2. ketosis can be induced using customary foods; 3. treatment with KD may be effective in controlling the progression of some gliomas; and 4. further studies are needed to determine factors that influence the effectiveness of KD, whether as a monotherapy, or as adjunctive or supplemental therapy in treating glioma patients.
Trial registration
ClinicalTrials.gov# NCT01535911 (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - March 25, 2015 Category: Cancer & Oncology Source Type: research
Pyruvate sensitizes pancreatic tumors to hypoxia-activated prodrug TH-302
Conclusions
Using metabolic profiling, functional imaging, and computational modeling, we show improved TH-302 activity by transiently increasing tumor hypoxia metabolically with exogenous pyruvate. Additionally, this work identified a set of biomarkers that may be used clinically to predict which tumors will be most responsive to pyruvate + TH-302 combination therapy. The results of this study support the concept that acute increases in tumor hypoxia can be beneficial for improving the clinical efficacy of HAPs and can positively impact the future treatment of PDAC and other cancers. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - January 29, 2015 Category: Cancer & Oncology Source Type: research
Mitochondria as biosynthetic factories for cancer proliferation
Abstract
Unchecked growth and proliferation is a hallmark of cancer, and numerous oncogenic mutations reprogram cellular metabolism to fuel these processes. As a central metabolic organelle, mitochondria execute critical biochemical functions for the synthesis of fundamental cellular components, including fatty acids, amino acids, and nucleotides. Despite the extensive interest in the glycolytic phenotype of many cancer cells, tumors contain fully functional mitochondria that support proliferation and survival. Furthermore, tumor cells commonly increase flux through one or more mitochondrial pathways, a...
Source: Cancer and Metabolism - January 25, 2015 Category: Cancer & Oncology Source Type: research
Erratum: The 2014 Beatson international cancer conference: powering the cancer machine
(Source: Cancer and Metabolism)
Source: Cancer and Metabolism - December 23, 2014 Category: Cancer & Oncology Source Type: research
Succinate dehydrogenase inhibition leads to epithelial-mesenchymal transition and reprogrammed carbon metabolism
Conclusions
These data illustrate how SDH dysfunction alters the epigenetic and metabolic landscape in ovarian cancer. By analyzing the involvement of this enzyme in transcriptional and metabolic networks, we find a metabolic Achilles’ heel that can be exploited therapeutically. Analyses of this type provide an understanding how specific perturbations in cancer metabolism may lead to novel anticancer strategies. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - December 15, 2014 Category: Cancer & Oncology Source Type: research
Quantitative analysis of acetyl-CoA production in hypoxic cancer cells reveals substantial contribution from acetate
Conclusions
Acetate is an important source of acetyl-CoA in hypoxia. Inhibition of acetate metabolism may impair tumor growth. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - December 11, 2014 Category: Cancer & Oncology Source Type: research
Acetate metabolism in cancer cells
(Source: Cancer and Metabolism)
Source: Cancer and Metabolism - December 11, 2014 Category: Cancer & Oncology Source Type: research
