How does the metabolism of tumour cells differ from that of normal cells

Amoêdo, Nívea Dias; Valencia, Juan P.; Rodrigues, M; Galina, Antônio; Rumjanek, Franklin David

doi:10.1042/bsr20130066

Cited by 70 publications

(58 citation statements)

References 48 publications

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“…It is known that the metabolic needs and intracellular signaling profiles of tumor cells differ from those of normal cells [50], and one or more compounds within AHCC might exploit this to effect Caspase-3-mediated apoptosis. Alternatively, tumor cells may express more AHCC-binding molecules and thereby bind one or more of the AHCC components.…”

Section: Discussionmentioning

confidence: 99%

Active hexose-correlated compound enhances extrinsic-pathway-mediated apoptosis of Acute Myeloid Leukemic cells

et al. 2017

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Active Hexose Correlated Compound (AHCC) has been shown to have many immunostimulatory and anti-cancer activities in mice and in humans. As a natural product, AHCC has potential to create safer adjuvant therapies in cancer patients. Acute Myeloid Leukemia (AML) is the least curable and second-most common leukemia in adults. AML is especially terminal to those over 60 years old, where median survival is only 5 to 10 months, due to inability to receive intensive chemotherapy. Hence, the purpose of this study was to investigate the effects of AHCC on AML cells both in vitro and in vivo. Results showed that AHCC induced Caspase-3-dependent apoptosis in AML cell lines as well as in primary AML leukopheresis samples. Additionally, AHCC induced Caspase-8 cleavage as well as Fas and TRAIL upregulation, suggesting involvement of the extrinsic apoptotic pathway. In contrast, monocytes from healthy donors showed suppressed Caspase-3 cleavage and lower cell death. When tested in a murine engraftment model of AML, AHCC led to significantly increased survival time and decreased blast counts. These results uncover a mechanism by which AHCC leads to AML-cell specific death, and also lend support for the further investigation of AHCC as a potential adjuvant for the treatment of AML.

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Section: Discussionmentioning

confidence: 99%

Active hexose-correlated compound enhances extrinsic-pathway-mediated apoptosis of Acute Myeloid Leukemic cells

et al. 2017

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“…Cancer cells need rapid ATP generation to maintain energy status, as well as an increase in the biosynthesis of macromolecules and the NADPH to maintain redox status (42). Tumor cells have a high glucose uptake through increased expression of GLUT transporters (5). Glucose upon entering the cell is phosphorylated by hexokinase forming glucose-6-phosphate.…”

Section: Discussionmentioning

confidence: 99%

“…The high collision energy (HCD) with MS/MS collision energies was set at 30 V and stepped NCE at 12.0%, nitrogen as the collision gas, and MS/MS spectra acquisition over a range of m/z values dependent on the precursor ion. Dynamic exclusion was set such that MS/MS for each precursor ion species was excluded for 4 s, under a fill ratio of 2.0%, an intensity threshold of 1.7e 5 , and an apex trigger of 2-5 s. All spectra were recorded in profile mode for further processing and analysis. Data Analysis-MS and MS/MS data analysis were carried out using Proteome Discoverer 1.4 software (version 1.4.0.288; Thermo Fisher Scientific) template that used both the Sequest search engine and an in-house Mascot 2.4.0 server (Matrix Science, London, UK).…”

Section: Methodsmentioning

confidence: 99%

Epithelial Mesenchymal Transition Induces Aberrant Glycosylation through Hexosamine Biosynthetic Pathway Activation

Lucena

Carvalho-Cruz

Donadio

et al. 2016

Journal of Biological Chemistry

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Deregulated cellular metabolism is a hallmark of tumors. Cancer cells increase glucose and glutamine flux to provide energy needs and macromolecular synthesis demands. Several studies have been focused on the importance of glycolysis and pentose phosphate pathway. However, a neglected but very important branch of glucose metabolism is the hexosamine biosynthesis pathway (HBP). The HBP is a branch of the glucose metabolic pathway that consumes ϳ2-5% of the total glucose, generating UDP-GlcNAc as the end product. UDP-GlcNAc is the donor substrate used in multiple glycosylation reactions. Thus, HBP links the altered metabolism with aberrant glycosylation providing a mechanism for cancer cells to sense and respond to microenvironment changes. Here, we investigate the changes of glucose metabolism during epithelial mesenchymal transition (EMT) and the role of O-GlcNAcylation in this process. We show that A549 cells increase glucose uptake during EMT, but instead of increasing the glycolysis and pentose phosphate pathway, the glucose is shunted through the HBP. The activation of HBP induces an aberrant cell surface glycosylation and O-GlcNAcylation. The cell surface glycans display an increase of sialylation ␣2-6, poly-LacNAc, and fucosylation, all known epitopes found in different tumor models. In addition, modulation of O-GlcNAc levels was demonstrated to be important during the EMT process. Taken together, our results indicate that EMT is an applicable model to study metabolic and glycophenotype changes during carcinogenesis, suggesting that cell glycosylation senses metabolic changes and modulates cell plasticity.Altered metabolism represents the first known difference between cancer cells and normal cells (1). The Warburg effect consists of an increase of glucose uptake for producing energy by a high rate of glycolysis followed by lactic acid fermentation even under high oxygen tension ("aerobic glycolysis"). Understanding the metabolism of tumors remains a topic of intense study with important therapeutic potential (2, 3). Several advances in cancer metabolism research over past years have enhanced our understanding of how aerobic glycolysis and other metabolic shifts support the anabolic demands of high growth rate (4). Traditionally, the study of glucose metabolism usually focused on the use of glucose for energy needs. However, cancer cells use glucose in anabolic pathways that provide precursors for the synthesis of lipids, proteins, glycans, and DNA to satisfy the demands of growth and proliferation. Several studies have been focused on the importance of the pentose phosphate pathway (PPP), 3 to generate NADPH that ensures the antioxidant defenses of the cell and to generate the nucleotides in high demand or the use of intermediates of the glycolytic pathway to generate molecules such as lipids or amino acids (5). However, a neglected but integral branch of glucose metabolism is the hexosamine biosynthesis pathway (HBP).Approximately 2-5% of glucose influx is directed to the HBP by the rate-limiting enzyme ...

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“…Many types of cancer result from significant changes in amino acid sequence due to metabolic changes in tumor cells [8]. The role of amino acids in cancer prevention is explored by scientists, and the use of these amino acid supplements is the part of alternative therapy which may helps slow progression of cancer.…”

Section: Introductionmentioning

confidence: 99%

Modeling of Cancer Classifier to Predict Site of Origin

Roy

Barman

2016

IEEE Trans.on Nanobioscience

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Cancer classification based on site of origin is very significant research issue for prediction and treatment of cancer. This paper is addressing the problem of cancer classification for Homo Sapiens genes composed of amino acid chain. Cancer gene network is realized by equivalent electrical circuits based on hydrophilic/ hydrophobic property of amino acid and a classifier is modeled to determine the cancer origin. The phase value, peak gain value and shape of Nyquist curve of network model are investigated to characterize different types of cancer gene origins. The model achieves 81.09% of classification accuracy and proves to be more sensitive and simple, since it shows 69% better performance compare to the existing nucleotide based method. The proposed classifier successfully predicts the site of origin of 93 cancer gene samples.

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How does the metabolism of tumour cells differ from that of normal cells

Cited by 70 publications

References 48 publications

Active hexose-correlated compound enhances extrinsic-pathway-mediated apoptosis of Acute Myeloid Leukemic cells

Active hexose-correlated compound enhances extrinsic-pathway-mediated apoptosis of Acute Myeloid Leukemic cells

Epithelial Mesenchymal Transition Induces Aberrant Glycosylation through Hexosamine Biosynthetic Pathway Activation

Modeling of Cancer Classifier to Predict Site of Origin

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