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6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase and tumor cell glycolysis.

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OBJECTIVE Neoplastic cells metabolize abundant glucose relative to normal cells in order to satisfy the increased energetic and anabolic needs of the transformed state. This review will summarize the requirement of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases for the regulation of

Role of tumor necrosis factor α (TNFα) in the onset of fructose-induced nonalcoholic fatty liver disease in mice.

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Tumor necrosis factor α (TNFα) is known to be involved in dysregulation of hepatic lipid metabolism and insulin signaling. However, whether TNFα also plays a casual role in the onset of fructose-induced nonalcoholic fatty liver disease (NAFLD) has not yet been determined. Therefore, wild-type and

Fructose 2,6-bisphosphate and the control of glycolysis by growth factors, tumor promoters and oncogenes.

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Tumor and proliferating cells maintain a high glycolytic rate even under aerobic conditions. The discovery of fructose 2,6-bisphosphate, a potent stimulator of glycolysis, has prompted a re-investigation of this phenomenon. Rat hepatoma cells and fibroblasts stimulated by mitogens or transformed by

Early detection of cancer cachexia in the rat using 31P magnetic resonance spectroscopy of the liver and a fructose stress test.

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The dynamic metabolic effects of a fructose infusion challenge on hepatic intracellular levels of adenosine 5'-triphosphate (ATP), inorganic phosphate (Pi) and phosphomonoesters (PME) were monitored noninvasively by 31P MRS in a remote tumour-bearing rat model. Fisher male rats were inoculated with

Metabolic depletion of ATP by fructose inversely controls CD95- and tumor necrosis factor receptor 1-mediated hepatic apoptosis.

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Hepatocyte apoptosis is crucial in several forms of liver disease. Here, we examined in different models of murine liver injury whether and how metabolically induced alterations of hepatocyte ATP levels control receptor-mediated apoptosis. ATP was depleted either in primary hepatocytes or in vivo by

Loss of fructose-1,6-bisphosphatase induces glycolysis and promotes apoptosis resistance of cancer stem-like cells: an important role in hexavalent chromium-induced carcinogenesis.

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Hexavalent chromium (Cr(VI)) compounds are confirmed human carcinogens for lung cancer. Our previous studies has demonstrated that chronic exposure of human bronchial epithelial BEAS-2B cells to low dose of Cr(VI) causes malignant cell transformation. The acquisition of cancer stem cell-like

Chinese medicine, Jiang-Tang-Ke-Li, improves insulin resistance by modulating muscle fiber composition and muscle tumor necrosis factor-alpha in fructose-fed rats.

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Insulin resistance and hyperinsulinemia are common findings in patients with essential hypertension. These impairments in glucose metabolism are commonly associated with diabetes mellitus, hypertension, and dyslipidemia, which are high risk factors of cardiovascular diseases, and recent evidence

Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells.

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Aberrant glycosylation is a universal feature of cancer cells, and certain glycan structures are well-known markers for tumor progression. Availability and composition of sugars in the microenvironment may affect cell glycosylation. Recent studies of human breast tumor cell lines indicate their

[Fructose-2,6-diphosphate and glycolysis of tumor cells].

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Tumour and proliferative cells maintain a high glycolytic rate even under aerobic conditions. The discovery of fructose-2,6-bisphosphate, a potent stimulator of glycolysis, has prompted a re-investigation of this phenomenon. Rat hepatoma cells and fibroblasts stimulated by mitogens or transformed by

Increased utilization of fructose has a positive effect on the development of breast cancer.

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Rapid proliferation and Warburg effect make cancer cells consume plenty of glucose, which induces a low glucose micro-environment within the tumor. Up to date, how cancer cells keep proliferating in the condition of glucose insufficiency still remains to be explored. Recent studies have revealed a

The role of fructose in metabolism and cancer.

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Fructose consumption has dramatically increased in the last 30 years. The principal form has been in the form of high-fructose corn syrup found in soft drinks and processed food. The effect of excessive fructose consumption on human health is only beginning to be understood. Fructose has been

Balancing glycolytic flux: the role of 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatases in cancer metabolism.

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The increased glucose metabolism in cancer cells is required to fulfill their high energetic and biosynthetic demands. Changes in the metabolic activity of cancer cells are caused by the activation of oncogenes or loss of tumor suppressors. They can also be part of the metabolic adaptations to the

Length vs. stiffness: which plays a dominant role in the cellular uptake of fructose-based rod-like micelles by breast cancer cells in 2D and 3D cell culture models?

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Polymeric nanoparticles with long circulation time hold great promise for anti-cancer drug delivery. An enhanced circulation effect of rod-like micelles has been reported, yet efficient intracellular delivery, especially their interactions with cells during endocytosis, still remains inconsistent.

Dietary Fructose Consumption and Triple-Negative Breast Cancer Incidence.

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In the past century the western world has found a way to combat most communicative diseases; however, throughout that time the prevalence of obesity, hyperglycemia, and hyperlipidemia have drastically increased. These symptoms characterize metabolic syndrome-a non-communicable disease which has

Protein kinase D3 promotes gastric cancer development through p65/6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 activation of glycolysis.

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Although serine/threonine-protein kinases are found to participate in a wide range of cancer progression, the involvement of protein kinase D3 (PRKD3) in gastric cancer has not been explored. Here, we investigated the role of PRKD3 in gastric cancer (GC) and its potential mechanisms. PRKD3 was

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