Stem cell factor and H<sub>2</sub>O<sub>2</sub> induce GLUT1 translocation in M07e cells

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

doi:10.1002/biof.5520200204

Cited by 19 publications

(19 citation statements)

References 37 publications

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“…Figure 2 shows that both the inhibitors diminish the phosphorylation increase induced by SCF and hydrogen peroxide. These results suggest that the activation of the SCF receptor, c-kit, is crucial for the signal pathways elicited by both stimuli and explain the ability of H 2 O 2 to mimic the action of SCF on glucose transport, previously reported (7,21). Cells were incubated in PBS at 37°C in the absence or presence of 5 µM ebselen or 1 µM radical probe [bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate] for 10 min and then treated with SCF (5 ng/ml) for an additional 10 min.…”

Section: Scf and H 2 O 2 Affect Glucose-transport Regulation Through mentioning

confidence: 72%

“…1). We previously observed that SCF and H 2 O 2 share the capability to promote Glut1 translocation to the cell membrane (21). We show that both SCF and H 2 O 2 lead to a c-kit-dependent increase in tyrosine phosphorylation and glucose transport.…”

Section: Signal Transduction and Gluti Regulation 275mentioning

confidence: 80%

“…These data suggest that both stimuli could share at least some signaling pathways leading to glucose-uptake activation, involving protein tyrosine kinases and PLC; H 2 O 2 could act by increasing the level of tyrosine phosphorylation through the inhibition of tyrosine phosphatases and mimicking the regulation role of endogenous ROS (21).…”

Section: Reactive Oxygen Species Cytokines and Glucose Transportmentioning

confidence: 96%

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

Maraldi

Fiorentini

Prata

et al. 2007

Antioxidants & Redox Signaling

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In leukemic cells, glucose transport is activated by SCF and H2O2 through a common signal cascade involving Akt, PLCgamma, Syk, and the Src family, in this order. An explanation can be provided by the phosphorylation of c-kit, the SCF receptor, elicited by either SCF or H2O2. Moreover, antioxidants prevent the SCF effect on glucose transport, confirming the involvement of H2O2 in the pathway leading to glucose-transport activation and suggesting a potential role for reactive oxygen species in leukemia proliferation.

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Section: Scf and H 2 O 2 Affect Glucose-transport Regulation Through mentioning

confidence: 72%

Section: Signal Transduction and Gluti Regulation 275mentioning

confidence: 80%

Section: Reactive Oxygen Species Cytokines and Glucose Transportmentioning

confidence: 96%

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

Maraldi

Fiorentini

Prata

et al. 2007

Antioxidants & Redox Signaling

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“…11,[20][21][22][23] These studies have implicated ROS as second messengers involved in mediating signaling from growth factors, such as granulocyte macrophage-colony stimulation factor (GM-CSF) and TPO. 11,20 With the use of a variety of oxidase inhibitors, these studies suggest that Nox's may be the source of ROS in these cell lineages.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of NADPH oxidases in megakaryocytes and their role in polyploidy

McCrann

Eliades

Makitalo

et al. 2009

Blood

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IntroductionMegakaryocytes (MKs) are platelet precursors in the bone marrow (BM) that undergo a complex maturation process called megakaryopoiesis. A hallmark of MK development occurs after their commitment to the MK lineage, in which MKs go through iterative rounds of endomitosis to become large polyploid cells. These cells can contain DNA content of up to and greater than 128N, with 2N being normal diploid DNA content. 1 The primary stimulus for progression of megakaryopoiesis is known to stem from thrombopoietin (TPO) signaling through the c-Mpl receptor 2 ; however, despite this being the focus of many studies, much of TPO signaling in MKs remains unclear.Recently, investigations of reactive oxygen species (ROS), their generation, and downstream signaling effects have shown that low physiologic levels of ROS play a role in promoting cell proliferation in many cells types, such as fibroblast, prostate, macrophage, endothelial, and vascular smooth muscle cells (VSMCs). 3-7 ROSproducing enzymes, such as a member of the NADPH oxidase (Nox) family, Nox1, have been described to be activated by mitogenic stimuli 8 and to produce ROS that have been shown to induce and maintain G 1 phase cyclin D1 expression in mouse lung epithelial cells. 9 Similarly, Havens et al 10 showed that ROSs increase in a cell cycle-dependent manner and oscillate with every cell division in human T98G glioblastoma cells, human leukemic T cells, and NIH 3T3 cells. Although, these investigators did not identify the source of ROS in these cells, they did show that on treatment with various antioxidants, cells undergo transient arrest and fail to make a timely G 1 -S phase progression. [11][12][13] In addition, Havens et al 10 described redox control over the activity of the anaphase promoting complex (APC) in association with Cdh1, mediating cyclin A degradation, a regulator of the G 1 /S transition. In the MK endomitotic cell cycle, cyclin D3 has been described as the predominant D-type cyclin that is up-regulated by TPO stimulation and induces high ploidy levels in cyclin D3 transgenic mice. 14-16 Ablation of cyclin D3 in cultured MKs results in a notable decrease in MK ploidy level, 16 although in vivo studies show a less dramatic effect on ploidy possibly because of compensation by other D cyclins. 17 Cyclin E is another G 1 phase cell-cycle regulator that has been suggested to play a role in MK ploidy promotion, notably inducing nonendomitotic megakaryoblastic K562 cells to undergo re-replication cycles. 18 The importance of cyclin E in promotion of ploidy is also supported by evidence from the cyclin E1 Ϫ/Ϫ E2 Ϫ/Ϫ double knockout (KO) mice produced with the use of the tetraploid complementation rescue method. 19 Interestingly, these mice developed normally with the exception of ploidy promotion in trophoblasts and MKs, showing a marked reduction in polyploid MKs even when cultured with TPO.To date, investigation of ROS in MKs has been limited to studies that used human megakaryocytic leukemic cell lines, such as MO7e and B1647 cells. 11,...

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“…We have previously demonstrated that NAD(P)H oxidasederived ROS are required for proliferation of acute leukemia cells, including self-producing VEGF cells (22,28,(33)(34)(35)(36)(37)(38)(39). However, significant work remains to be performed to define the role of each Nox isoform and its regulatory subunits, and to identify molecular targets of oxidase-derived ROS involved in proliferation/viability of leukemic cells.…”

Section: Discussionmentioning

confidence: 99%

VEGF-induced ROS generation from NAD(P)H oxidases protects human leukemic cells from apoptosis

Maraldi

Prata²,

Caliceti³

et al. 2010

Int J Oncol

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Abstract. Vascular endothelial growth factor (VEGF) and reactive oxygen species (ROS) play critical roles in vascular pathophysiology and in hematological malignancies. VEGF is supposed to utilize ROS as messenger intermediates downstream of the VEGF receptor-2. NAD(P)H oxidase (Nox) family is a major source of cellular ROS and is implicated in increased ROS production in tumor cells. We previously demonstrated that B1647 cells, a human leukemic cell line, express Nox2 and Nox4, both at mRNA and protein level. We suggest here that the VEGF-induced increase in ROS can be related to Nox2 and Nox4 activities. Nox-derived ROS are involved in early signaling events such as the autophosphorylation of VEGF receptor-2, and in the modulation of glucose uptake, a cellular activity strictly bound to VEGFinduced leukemic cell proliferation, as shown by experiments with antioxidants and Nox inhibitors and siRNA. Noxgenerated ROS are required to sustain B1647 cell viability and proliferation; in fact, antioxidants such as EUK-134 or Nox inhibitors and siRNA direct cells to apoptotic cell death, suggesting that manipulation of cellular Nox2 and Nox4 could affect survival of leukemic cells.

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Stem cell factor and H₂O₂ induce GLUT1 translocation in M07e cells

Cited by 19 publications

References 37 publications

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

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

Differential expression of NADPH oxidases in megakaryocytes and their role in polyploidy

VEGF-induced ROS generation from NAD(P)H oxidases protects human leukemic cells from apoptosis

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Stem cell factor and H2O2 induce GLUT1 translocation in M07e cells

Cited by 19 publications

References 37 publications

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

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

Differential expression of NADPH oxidases in megakaryocytes and their role in polyploidy

VEGF-induced ROS generation from NAD(P)H oxidases protects human leukemic cells from apoptosis

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Stem cell factor and H₂O₂ induce GLUT1 translocation in M07e cells

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

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