Regulation of interleukin-8 expression by reduced oxygen pressure in human glioblastoma

Desbaillets, Isabelle; Diserens, Annie‐Claire; Tribolet, Nicolas de; Hamou, Marie‐France; Meir, Erwin G. Van

doi:10.1038/sj.onc.1202424

Cited by 103 publications

(69 citation statements)

References 39 publications

(31 reference statements)

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“…SDF-1 stimulation of human endothelial cells induces the production of the angiogenic factor vascuilar endothelial growth factor (68), while in this study, we have shown that SDF-1 induces IL-8 production by astroglioma cells. Both of these angiogenic factors are increased in brain tumors (69,70). At present, the contribution of IL-8 to CNS angiogenesis is unclear.…”

Section: Discussionmentioning

confidence: 99%

CXC Chemokine Receptor 4 Expression and Function in Human Astroglioma Cells

Drabik

Kutsch

et al. 2001

The Journal of Immunology

104

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Chemokines constitute a superfamily of proteins that function as chemoattractants and activators of leukocytes. Astrocytes, the major glial cell type in the CNS, are a source of chemokines within the diseased brain. Specifically, we have shown that primary human astrocytes and human astroglioma cell lines produce the CXC chemokines IFN-γ-inducible protein-10 and IL-8 and the CC chemokines monocyte chemoattractant protein-1 and RANTES in response to stimuli such as TNF-α, IL-1β, and IFN-γ. In this study, we investigated chemokine receptor expression and function on human astroglioma cells. Enhancement of CXC chemokine receptor 4 (CXCR4) mRNA expression was observed upon treatment with the cytokines TNF-α and IL-1β. The peak of CXCR4 expression in response to TNF-α and IL-1β was 8 and 4 h, respectively. CXCR4 protein expression was also enhanced upon treatment with TNF-α and IL-1β (2- to 3-fold). To study the functional relevance of CXCR4 expression, stable astroglioma transfectants expressing high levels of CXCR4 were generated. Stimulation of cells with the ligand for CXCR4, stromal cell-derived factor-1α (SDF-1α), resulted in an elevation in intracellular Ca2+ concentration and activation of the mitogen-activated protein kinase cascade, specifically, extracellular signal-regulated kinase 2 (ERK2) mitogen-activated protein kinase. Of most interest, SDF-1α treatment induced expression of the chemokines monocyte chemoattractant protein-1, IL-8, and IFN-γ-inducible protein-10. SDF-1α-induced chemokine expression was abrogated upon inclusion of U0126, a pharmacological inhibitor of ERK1/2, indicating that the ERK signaling cascade is involved in this response. Collectively, these data suggest that CXCR4-mediated signaling pathways in astroglioma cells may be another mechanism for these cells to express chemokines involved in angiogenesis and inflammation.

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Section: Discussionmentioning

confidence: 99%

CXC Chemokine Receptor 4 Expression and Function in Human Astroglioma Cells

Drabik

Kutsch

et al. 2001

The Journal of Immunology

104

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“…The analysis of the MIC-1 gene promoter revealed the presence of putative consensus sequences for several transcription factors, including AP-1 and, Sp1 and Sp3 (Baek et al, 2001a;Bottner et al, 1999;Lawton et al, 1997). AP-1 has been shown previously to act as an anoxic stress mediator in glioblastoma cell lines LN-229 and LN-Z308 (Desbaillets et al, 1999) and might be a possible candidate in anoxia mediated MIC-1 up-regulation. However, it remains to be seen whether modulation of MIC-1 represents a specific response to anoxia or rather a secondary effect of anoxia, such as ATP depletion and cell injury.…”

Section: Discussionmentioning

confidence: 99%

“…The cell lines were subjected to anoxia using an Oxoid Gas generating anaerobic chamber (Unipath Ltd, Hampshire, UK) as described (Desbaillets et al, 1999). Cobalt chloride treatment was performed by incubating cells with cobalt chloride at different concentrations (100, 200 or 400 mM) for 24 h (Tenan et al, 2000).…”

Section: Methodsmentioning

confidence: 99%

Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1

et al. 2002

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“…In fact, several cell types including tumor cells, macrophages, and endothelial cells respond to hypoxia by producing angiogenic factors, fibrinolytic factors, and adhesion molecules involved in pathologic angiogenesis (1)(2)(3)(4)(5). Four sequential steps can be distinguished during angiogenesis: the degradation of the basement membrane and interstitial matrix, endothelial cell migration, endothelial cell proliferation, and the formation of tubular structures with a lumen and a new basement membrane (6).…”

mentioning

confidence: 99%

“…Three of these steps critically depend on proteolytic activity generated by the matrix metalloproteinases and the plasminogen activator/plasmin system. In particular, the role of urokinase plasminogen activator receptor (uPAR) 1 in tumor cell invasion and migration and in the formation of new microvascular structures has been largely demonstrated (7)(8)(9).…”

mentioning

confidence: 99%

bcl-2 Induction of Urokinase Plasminogen Activator Receptor Expression in Human Cancer Cells through Sp1 Activation

Trisciuoglio¹,

Iervolino²,

Candiloro³

et al. 2004

Journal of Biological Chemistry

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We have previously demonstrated that Bcl-2 overexpression in human breast carcinoma and melanoma cells synergizes with hypoxia to increase angiogenesis through up-regulation of vascular endothelial growth factor. In this work we demonstrated, for the first time, that Bcl-2 overexpression in cancer cells exposed to hypoxia modulates urokinase plasminogen activator receptor (uPAR) expression through Sp1 transcription factor and that the extracellular signal-regulated kinase (ERK) pathway plays a role in Sp1 transcriptional activity. In particular, an increase in uPAR protein and mRNA expression was found in melanoma bcl-2 transfectants grown under hypoxia when compared with control cells, and a decrease of uPAR protein expression was induced by treatment of cells with specific bcl-2 antisense oligonucleotides. Up-regulation of uPAR expression was accompanied by increased Sp1 protein expression, stability, serine phosphorylation, and DNA binding activity. Treatment of cells with mitramycin A, an inhibitor of Sp1 activity, confirmed the role of Sp1 transcriptional activity in uPAR induction by Bcl-2. The contribution of the ERK pathway in Sp1-increased transcriptional activity was demonstrated by the use of chemical inhibition. In fact, ERK kinase activation was induced in Bcl-2-overexpressing cells exposed to hypoxia, and the ERK kinase inhibitor UO126 was able to down-regulate Sp1 phosphorylation and DNA binding activity. Using a human breast carcinoma line, we obtained data supporting our findings with melanoma cells and identified a link between the induction of Sp1 and uPAR expression as a common bcl-2-controlled phenomenon in human tumors. In conclusion, our results strongly indicate that up-regulation of uPAR expression by Bcl-2 in hypoxia is modulated by Sp1 DNA binding activity through the ERK signaling pathway.Angiogenesis is a fundamental process required for tumor growth, invasion, and metastasis and is strongly induced by hypoxia. In fact, several cell types including tumor cells, macrophages, and endothelial cells respond to hypoxia by producing angiogenic factors, fibrinolytic factors, and adhesion molecules involved in pathologic angiogenesis (1-5). Four sequential steps can be distinguished during angiogenesis: the degradation of the basement membrane and interstitial matrix, endothelial cell migration, endothelial cell proliferation, and the formation of tubular structures with a lumen and a new basement membrane (6). Three of these steps critically depend on proteolytic activity generated by the matrix metalloproteinases and the plasminogen activator/plasmin system. In particular, the role of urokinase plasminogen activator receptor (uPAR) 1 in tumor cell invasion and migration and in the formation of new microvascular structures has been largely demonstrated (7-9).Angiogenesis is also controlled by alterations in oncogene and tumor suppressor gene expression (10 -14). In this context, we previously demonstrated that the bcl-2 oncogene increases in vitro and in vivo angiogenesis in two different t...

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Regulation of interleukin-8 expression by reduced oxygen pressure in human glioblastoma

Cited by 103 publications

References 39 publications

CXC Chemokine Receptor 4 Expression and Function in Human Astroglioma Cells

CXC Chemokine Receptor 4 Expression and Function in Human Astroglioma Cells

Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1

bcl-2 Induction of Urokinase Plasminogen Activator Receptor Expression in Human Cancer Cells through Sp1 Activation

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