Glucose-Transport Regulation in Leukemic Cells: How Can H<sub>2</sub>O<sub>2</sub> Mimic Stem Cell Factor Effects?

Maraldi, Tullia; Fiorentini, Diana; Prata, Cecilia; Landi, Laura; Hakim, Gabriele

doi:10.1089/ars.2007.9.271

Cited by 12 publications

(14 citation statements)

References 28 publications

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“…Moreover, the high proliferative capacity of murine embryonic stem cells was shown to be closely correlated with the high activity of different glycolytic enzymes, elevated glycolytic flux, and low mitochondrial oxygen consumption (25). In leukemic cells, glucose transport is activated by stem cell factor and H 2 O 2 , suggesting a potential role for ROS in leukemia proliferation (29). NADPH oxidase plays an important role in promoting the proliferation of skeletal muscle precursor cells (30).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Gurusamy

Mukherjee

Lekli

et al. 2009

Antioxidants & Redox Signaling

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Redox effector protein-1 (Ref-1) plays an essential role in DNA repair and redox regulation of several transcription factors. In the present study, we examined the role of Ref-1 in maintaining the redox status and survivability of adult cardiac stem cells challenged with a subtoxic level of H2O2 under inhibition of Ref-1 by RNA interference. Treatment of cardiac stem cells with a low concentration of H2O2 induced Ref-1-mediated survival signaling through phosphorylation of Akt. However, Ref-1 inhibition followed by H2O2 treatment extensively induced the level of intracellular reactive oxygen species (ROS) through activation of the components of NADPH oxidase, like p22( phox ), p47( phox ), and Nox4. Cardiac differentiation markers (Nkx2.5, MEF2C, and GATA4), and cell death by apoptosis were significantly elevated in Ref-1 siRNA followed by H2O2-treated stem cells. Further, inhibition of Ref-1 increased the level of p53 but decreased the phosphorylation of Akt, a molecule involved in survival signaling. Treatment with ROS scavenger N-acetyl-L-cysteine attenuated Ref-1 siRNA-mediated activation of NADPH oxidase and cardiac differentiation. Taken together, these results indicate that Ref-1 plays an important role in maintaining the redox status of cardiac stem cells and protects them from oxidative injury-mediated cell death and differentiation.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Gurusamy

Mukherjee

Lekli

et al. 2009

Antioxidants & Redox Signaling

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“…Cell viability was also assayed by the MTT assay [23], since the reduction of tetrazolium salts is widely accepted as a reliable way to examine cell viability/proliferation. Cells were incubated with 0.5 mg/mL MTT for 4 h at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Role of Plasma Membrane Caveolae/Lipid Rafts in VEGF-Induced Redox Signaling in Human Leukemia Cells

Caliceti

Zambonin

Rizzo

et al. 2014

BioMed Research International

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Caveolae/lipid rafts are membrane-rich cholesterol domains endowed with several functions in signal transduction and caveolin-1 (Cav-1) has been reported to be implicated in regulating multiple cancer-associated processes, ranging from tumor growth to multidrug resistance and angiogenesis. Vascular endothelial growth factor receptor-2 (VEGFR-2) and Cav-1 are frequently colocalized, suggesting an important role played by this interaction on cancer cell survival and proliferation. Thus, our attention was directed to a leukemia cell line (B1647) that constitutively produces VEGF and expresses the tyrosine-kinase receptor VEGFR-2. We investigated the presence of VEGFR-2 in caveolae/lipid rafts, focusing on the correlation between reactive oxygen species (ROS) production and glucose transport modulation induced by VEGF, peculiar features of tumor proliferation. In order to better understand the involvement of VEGF/VEGFR-2 in the redox signal transduction, we evaluated the effect of different compounds able to inhibit VEGF interaction with its receptor by different mechanisms, corroborating the obtained results by immunoprecipitation and fluorescence techniques. Results here reported showed that, in B1647 leukemia cells, VEGFR-2 is present in caveolae through association with Cav-1, demonstrating that caveolae/lipid rafts act as platforms for negative modulation of VEGF redox signal transduction cascades leading to glucose uptake and cell proliferation, suggesting therefore novel potential targets.

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“…It has recently been reported that in a human neuronal cell line, SH-SY5Y, GLUT1 translocation in response to insulin-like growth factor (IGF-I) occurs [27] and, for the first time in a neuronal cell system, also GLUT4 is translocated to the plasma membrane in response to insulin [28]. We have been studying for a long time the glucose transport activity in many leukaemia cell lines expressing mainly GLUT1, demonstrating that, also in these cell types, GLUT1 is recruited on the plasma membrane from intracellular compartments in response to different stimuli, greatly enhancing the rate of glucose uptake [29, 30]. Moreover, it is well known that impaired GLUT4 translocation is causally linked to insulin resistance and consequently to noninsulin-dependent diabetes mellitus [31, 32].…”

Section: Introductionmentioning

confidence: 99%

Steviol Glycosides Modulate Glucose Transport in Different Cell Types

Rizzo

Zambonin

Angeloni

et al. 2013

Oxidative Medicine and Cellular Longevity

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Extracts from Stevia rebaudiana Bertoni, a plant native to Central and South America, have been used as a sweetener since ancient times. Currently, Stevia extracts are largely used as a noncaloric high-potency biosweetener alternative to sugar, due to the growing incidence of type 2 diabetes mellitus, obesity, and metabolic disorders worldwide. Despite the large number of studies on Stevia and steviol glycosides in vivo, little is reported concerning the cellular and molecular mechanisms underpinning the beneficial effects on human health. The effect of four commercial Stevia extracts on glucose transport activity was evaluated in HL-60 human leukaemia and in SH-SY5Y human neuroblastoma cells. The extracts were able to enhance glucose uptake in both cellular lines, as efficiently as insulin. Our data suggest that steviol glycosides could act by modulating GLUT translocation through the PI3K/Akt pathway since treatments with both insulin and Stevia extracts increased the phosphorylation of PI3K and Akt. Furthermore, Stevia extracts were able to revert the effect of the reduction of glucose uptake caused by methylglyoxal, an inhibitor of the insulin receptor/PI3K/Akt pathway. These results corroborate the hypothesis that Stevia extracts could mimic insulin effects modulating PI3K/Akt pathway.

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Glucose-Transport Regulation in Leukemic Cells: How Can H₂O₂ Mimic Stem Cell Factor Effects?

Cited by 12 publications

References 28 publications

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Role of Plasma Membrane Caveolae/Lipid Rafts in VEGF-Induced Redox Signaling in Human Leukemia Cells

Steviol Glycosides Modulate Glucose Transport in Different Cell Types

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Glucose-Transport Regulation in Leukemic Cells: How Can H2O2 Mimic Stem Cell Factor Effects?

Cited by 12 publications

References 28 publications

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Inhibition of Ref-1 Stimulates the Production of Reactive Oxygen Species and Induces Differentiation in Adult Cardiac Stem Cells

Role of Plasma Membrane Caveolae/Lipid Rafts in VEGF-Induced Redox Signaling in Human Leukemia Cells

Steviol Glycosides Modulate Glucose Transport in Different Cell Types

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Glucose-Transport Regulation in Leukemic Cells: How Can H₂O₂ Mimic Stem Cell Factor Effects?