Glucose metabolism in cancer cells

@article{Annibaldi2010GlucoseMI,
  title={Glucose metabolism in cancer cells},
  author={Alessandro Annibaldi and Christian Widmann},
  journal={Current Opinion in Clinical Nutrition and Metabolic Care},
  year={2010},
  volume={13},
  pages={466–470}
}
  • A. Annibaldi, C. Widmann
  • Published 2010
  • Biology, Medicine
  • Current Opinion in Clinical Nutrition and Metabolic Care
Purpose of reviewCancer cells alter their metabolism in order to support their rapid proliferation and expansion across the body. In particular, tumor cells, rather than fueling glucose in the oxidative phosphorylation pathway, generally use glucose for aerobic glycolysis. In this review, we discuss some of the mechanisms thought to be responsible for the acquisition of a glycolytic phenotype in cancer cells and how the switch towards glycolysis represents a selective growth advantage. Recent… Expand
Dysregulation of Glucose Metabolism by Oncogenes and Tumor Suppressors in Cancer Cells
TLDR
This review summarizes the roles of tumor suppressors and oncogenes and their products that provide metabolic advantages to cancer cells which in turn leads to the establishment of the “Warburg effect” and ultimately leads to cancer progression. Expand
Cancer stem cell metabolism: a potential target for cancer therapy
TLDR
This review describes the key metabolic pathways required by CSCs to maintain a survival advantage and highlights how a combined approach of targeting cellular metabolism in conjunction with the use of chemotherapeutic drugs may provide a promising strategy to overcome therapeutic resistance and therefore aid in cancer therapy. Expand
Cancer Stem Cell Metabolism and Potential Therapeutic Targets
TLDR
Key factors that impact CSC metabolic phenotype including heterogeneity of CSCs across different histologic tumor types, tissue-specific variations, tumor microenvironment, and CSC niche are reviewed including targeting key players of glycolytic and mitochondrial pathways. Expand
Metabolic implication of tumor:stroma crosstalk in breast cancer
TLDR
The aim of this review is to gather the most recent data regarding the metabolic alterations in breast cancer, describe the role of tumor microenvironment in Breast cancer cell metabolic reprogramming, and contemplate how targeting metabolic pathways aberrantly activated in breast cancers could help current therapeutic regimens. Expand
Energy Metabolism in H460 Lung Cancer Cells: Effects of Histone Deacetylase Inhibitors
TLDR
NaB and TSA induced an increase in mitochondrial function and oxidative metabolism in H460 lung tumor cells concomitant with a less proliferative cellular phenotype. Expand
Computational modeling to determine key regulators of hypoxia effects on the lactate production in the glycolysis pathway
TLDR
A quantitative relationship between the hypoxia intensity and the intracellular lactate levels is established and the key regulators of the glycolysis pathway are determined and it is predicted that the phosphofructokinase-1 and phosphoglucomutase enzymes might play the most important roles in the regulation of the lactate production. Expand
Metformin is synthetically lethal with glucose withdrawal in cancer cells
TLDR
The microenvironment-mediated contextual synthetic lethality of metformin should be expected to enormously potentiate the anti-cancer effect of anti-angiogenesis agents that promote severe oxygen and glucose deprivation in certain areas of the tumor tissues. Expand
Lactic acid induces lactate transport and glycolysis/OXPHOS interconversion in glioblastoma.
TLDR
Under glucose deprivation, lactic acid can preserve high ATP levels and resist cell death in U251 cells and convert the dominant Warburg effect to OXPHOS, which may promote the development of new therapeutic strategies in GBM. Expand
Central role of lactic acidosis in cancer cell resistance to glucose deprivation‐induced cell death
TLDR
The ability of cancer cells to resist glucose deprivation‐induced cell death is conferred, at least in part, by lactic acidosis, and it is envisioned that disrupting the lactic Acidosis may resume the sensitivity ofcancer cells to glucose deprivation. Expand
Dibenzophenanthridines as Inhibitors of Glutaminase C and Cancer Cell Proliferation
TLDR
It is found that the hot-spot ring must be substituted with a large, nonplanar functionality to bestow activity to the series, leading to a model whereby the molecule binds glutaminase at a previously undescribed allosteric site. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 55 REFERENCES
Energy metabolism in tumor cells
TLDR
It is proposed that energy metabolism may be an alternative therapeutic target for both hypoxic (glycolytic) and oxidative tumors. Expand
Akt Stimulates Aerobic Glycolysis in Cancer Cells
TLDR
It is suggested that activation of the Akt oncogene is sufficient to stimulate the switch to aerobic glycolysis characteristic of cancer cells and that Akt activity renders cancer cells dependent on aerobic glyCOlysis for continued growth and survival. Expand
Metabolic catastrophe as a means to cancer cell death
TLDR
Tumor cells cannot adapt efficiently to metabolic stress and could be induced to die by metabolic catastrophe, in which high energy demand is contrasted by insufficient energy production. Expand
Roles of p53, Myc and HIF-1 in Regulating Glycolysis — the Seventh Hallmark of Cancer
TLDR
The underlying mechanisms leading to the Warburg phenomenon include mitochondrial changes, upregulation of rate-limiting enzymes/proteins in glycolysis and intracellular pH regulation, hypoxia-induced switch to anaerobic metabolism, and metabolic reprogramming after loss of p53 function. Expand
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TLDR
It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell. Expand
Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells
TLDR
Studying the transcriptomes of paired colorectal cancer cell lines that differed only in the mutational status of their KRAS or BRAF genes, it is suggested that glucose deprivation can drive the acquisition of KRAS pathway mutations in human tumors. Expand
Why do cancers have high aerobic glycolysis?
TLDR
It is proposed that persistent metabolism of glucose to lactate even in aerobic conditions is an adaptation to intermittent hypoxia in pre-malignant lesions, which leads to microenvironmental acidosis requiring evolution to phenotypes resistant to acid-induced cell toxicity. Expand
Cellular adaptations to hypoxia and acidosis during somatic evolution of breast cancer
TLDR
Adaptation to hypoxia and acidosis may represent key events in transition from in situ to invasive cancer and be critical for emergence of invasive cancer. Expand
The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid β-oxidation
TLDR
It is suggested that activation of Akt blocks the ability of cancer cells to metabolize nonglycolytic bioenergetic substrates, leading to glucose addiction. Expand
Glucose catabolism in cancer cells: amplification of the gene encoding type II hexokinase.
TLDR
It is demonstrated by Southern blot analysis and fluorescence in situ hybridization that in the rapidly growing rat AS-30D hepatoma cell line, enhanced hexokinase activity is associated with at least a 5-fold amplification of the type II gene relative to normal hepatocytes. Expand
...
1
2
3
4
5
...