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See detailNF-kappaB activation in endothelial cells is critical for the activity of angiostatic agents.
Tabruyn, Sébastien ULg; Memet, Sylvie; Ave, Patrick et al

in Molecular Cancer Therapeutics (2009), 8(9), 2645-54

In tumor cells, the transcription factor NF-kappaB has been described to be antiapoptotic and proproliferative and involved in the production of angiogenic factors such as vascular endothelial growth ... [more ▼]

In tumor cells, the transcription factor NF-kappaB has been described to be antiapoptotic and proproliferative and involved in the production of angiogenic factors such as vascular endothelial growth factor. From these data, a protumorigenic role of NF-kappaB has emerged. Here, we examined in endothelial cells whether NF-kappaB signaling pathway is involved in mediating the angiostatic properties of angiogenesis inhibitors. The current report describes that biochemically unrelated agents with direct angiostatic effect induced NF-kappaB activation in endothelial cells. Our data showed that endostatin, anginex, angiostatin, and the 16-kDa N-terminal fragment of human prolactin induced NF-kappaB activation in endothelial cells in both cultured human endothelial cells and in vivo in a mouse tumor model. It was also found that NF-kappaB activity was required for the angiostatic activity, because inhibition of NF-kappaB in endothelial cells impaired the ability of angiostatic agents to block sprouting of endothelial cells and to overcome endothelial cell anergy. Therefore, activation of NF-kappaB in endothelial cells can result in an unexpected antitumor outcome. Based on these data, the current approach of systemic treatment with NF-kappaB inhibitors may therefore be revisited because NF-kappaB activation specifically targeted to endothelial cells might represent an efficient strategy for the treatment of cancer. [less ▲]

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See detailNf-Kappab Activation in Response to Toxical and Therapeutical Agents: Role in Inflammation and Cancer Treatment
Bours, Vincent ULg; Bonizzi, Giuseppina; Bentires-Alj, Mohamed et al

in Toxicology (2000), 153(1-3), 27-38

The NF-kappaB transcription factor is ubiquitously expressed and controls the expression of a large number of genes. Experimental data clearly indicate that NF-kappaB is a major regulator of the ... [more ▼]

The NF-kappaB transcription factor is ubiquitously expressed and controls the expression of a large number of genes. Experimental data clearly indicate that NF-kappaB is a major regulator of the inflammatory reaction by controlling the expression of pro-inflammatory molecules in response to cytokines, oxidative stress and infectious agents. We demonstrated that NF-kappaB activation by IL-1beta follows three distinct cell-specific pathways. Moreover, our studies indicated that in one model of inflammatory diseases, horse recurrent airway obstruction (RAO), the extent of NF-kappaB basal activity correlates with pulmonary dysfunction. Another role of NF-kappaB activity protects cancer cells against apoptosis and could participate in the resistance to cancer treatment. However, we did not observe any increased cytotoxicity after treatment with anticancer drugs or TNF-alpha of cells expressing a NF-kappaB inhibitor. Therefore, we can conclude that the inhibition of apoptosis by NF-kappaB is likely to be cell type and stimulus-dependent. Further studies are required to determine whether NF-kappaB could be a target for anticancer treatments. [less ▲]

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See detailNF-kappaB inhibition improves the sensitivity of human glioblastoma cells to 5-aminolevulinic acid-based photodynamic therapy.
Coupienne, Isabelle ULg; Bontems, Sébastien ULg; Dewaele, M. et al

in Biochemical Pharmacology (2011)

Glioblastoma constitute the most frequent and deadliest brain tumors of astrocytic origin. They are very resistant to all current therapies and are associated with a huge rate of recurrence. In most cases ... [more ▼]

Glioblastoma constitute the most frequent and deadliest brain tumors of astrocytic origin. They are very resistant to all current therapies and are associated with a huge rate of recurrence. In most cases, this type of tumor is characterized by a constitutive activation of the nuclear factor-kappaB (NF-kappaB). This factor is known to be a key regulator of various physiological processes such as inflammation, immune response, cell growth or apoptosis. In the present study, we explored the role of NF-kappaB activation in the sensitivity of human glioblastoma cells to a treatment by 5-aminolevulinic acid (5-ALA)-based photodynamic therapy (PDT). 5-ALA is a physiological compound widely used in PDT as well as in tumor photodetection (PDD). Our results show that inhibition of NF-kappaB improves glioblastoma cell death in response to 5-ALA-PDT. We then studied the molecular mechanisms underlying the cell death induced by PDT combined or not with NF-kappaB inhibition. We found that apoptosis was induced by PDT but in an incomplete manner and that, unexpectedly, NF-kappaB inhibition reduced its level. Oppositely PDT mainly induces necrosis in glioblastoma cells and NF-kappaB is found to have anti-necrotic functions in this context. The autophagic flux was also enhanced as a result of 5-ALA-PDT and we demonstrate that stimulation of autophagy acts as a pro-survival mechanism confering protection against PDT-mediated necrosis. These data point out that 5-ALA-PDT has an interesting potential as a mean to treat glioblastoma and that inhibition of NF-kappaB renders glioblastoma cells more sensitive to the treatment. [less ▲]

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See detailNF-kappaB transcription factor activation by hydrogen peroxide can be decreased by 2,3-dihydroxybenzoic acid and its ethylester derivative
Sappey, Christine; Boelaert, J. R.; Legrand-Poels, Sylvie ULg et al

in Archives of Biochemistry & Biophysics (1995)

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See detailNF-kappaB transcription factor and human immunodeficiency virus type 1 (HIV-1) are activated by methylene blue photosensitization
Piret, Bernard; Legrand-Poels, Sylvie ULg; Sappey, Christine et al

in European Journal of Biochemistry (1995)

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See detailThe NF-kappaB transcription factor: structure, function and interaction with the oncoprotein Bcl-3.
Bours, Vincent ULg

Thèse d’agrégation de l’enseignement supérieur (1994)

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See detailNF-kappaB: an important transcription factor in photobiology
Legrand-Poels, Sylvie ULg; Schoonbroodt, Sonia; Matroule, Jean-Yves et al

in Journal of Photochemistry and Photobiology B : Biology (1998)

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See detailNF-kB activity, and IL-8 and GM-CSF expression, in the milk of chorionic mastitis-affected cows
Boulanger, Delphine; Bureau, Fabrice ULg; Lekeux, Pierre ULg

in Pflügers Archiv : European Journal of Physiology (2002), 443

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See detailNF-kB activity, and IL-8 and GM-CSF expression, in the milk of chorionic mastitis-affected cows
Boulanger, Delphine; Bureau, Fabrice ULg; Lekeux, Pierre ULg

in National Mastitis Council Proceedings (2002)

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See detailNF-kB activity, and IL-8 and GM-CSF expression, in the milk of chronic mastitis-affected cows
Boulanger, D.; Bureau, Fabrice ULg; Lekeux, Pierre ULg

in Proceedings : National Mastitis Council, 41st Annual Meeting (2002)

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See detailNF-kB, stem cells and breast cancer: the links get stronger
Shostak, Kateryna ULg; Chariot, Alain ULg

in Breast Cancer Research [=BCR] (2011), 13(4), 214

Self-renewing breast cancer stem cells are key actors in perpetuating tumour existence and in treatment resistance and relapse. The molecular pathways required for their maintenance are starting to be ... [more ▼]

Self-renewing breast cancer stem cells are key actors in perpetuating tumour existence and in treatment resistance and relapse. The molecular pathways required for their maintenance are starting to be elucidated. Among them is the transcription factor NF-κB, which is known to play critical roles in cell survival, inflammation and immunity. Recent studies indicate that mammary epithelial NF-κB regulates the self-renewal of breast cancer stem cells in a model of Her2-dependent tumourigenesis. We will describe here the NF-κB-activating pathways that are involved in this process and in which progenitor cells this transcription factor is actually activated. [less ▲]

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See detailNF-kB-dependent cytokine production is abolished by cyclopentenone prostaglandins in lung epithelial cells
Bureau, Fabrice ULg

in Proceedings: Annual Congress of the European Respiratory Society (2001)

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See detailThe NF-κ B-independent functions of IKK subunits in immunity and cancer
Chariot, Alain ULg

in Trends in Cell Biology (2009), 19

The IKK complex is involved in transcriptional activation by phosphorylating the inhibitory molecule IkBa, a modification that triggers its subsequent degradation, allowing activation of NF-kB ... [more ▼]

The IKK complex is involved in transcriptional activation by phosphorylating the inhibitory molecule IkBa, a modification that triggers its subsequent degradation, allowing activation of NF-kB. Importantly, recent reports indicate that multiple cytoplasmic and nuclear proteins distinct from the NF-kB/IkB proteins are phosphorylated by the catalytic subunits of the IKK complex, IKKa or IKKb. Here we describe how the IKK subunits can play crucial roles in allergy, inflammation, immunity by targeting proteins such as SNAP23 and IRF7 but also in cancer by phosphorylating key molecules such as p53, TSC1 and FOXO3a through NF-kB-independent pathways. Thus, these recent findings considerably widen the biological roles played by these kinases and suggest that a full understanding of the biological roles played by IKKa and IKKb requires an exhaustive characterization of their substrates. [less ▲]

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See detailNF-κB transcription factor induces drug resistance through MDR1 expression in cancer cells
Bentires-Alj, Mohamed; Barbu, Véronique; Fillet, Marianne ULg et al

in Oncogene (2003), 22

The ubiquitous NF-kappaB transcription factor has been reported to inhibit apoptosis and to induce drug resistance in cancer cells. Drug resistance is the major reason for cancer therapy failure and ... [more ▼]

The ubiquitous NF-kappaB transcription factor has been reported to inhibit apoptosis and to induce drug resistance in cancer cells. Drug resistance is the major reason for cancer therapy failure and neoplastic cells often develop multiple mechanisms of drug resistance during tumor progression. We observed that NF-kappaB or P-glycoprotein inhibition in the HCT15 colon cancer cells led to increased apoptotic cell death in response to daunomycin treatment. Interestingly, NF-kappaB inhibition through transfection of a plasmid coding for a mutated IkappaB-alpha inhibitor increased daunomycin cell uptake. Indeed, the inhibition of NF-kappaB reduced mdr1 mRNA and P-glycoprotein expression in HCT15 cells. We identified a consensus NF-kappaB binding site in the first intron of the human mdr1 gene and demonstrated that NF-kappaB complexes could bind with this intronic site. Moreover, NF-kappaB transactivates an mdr1 promoter luciferase construct. Our data thus demonstrate a role for NF-kappaB in the regulation of the mdr1 gene expression in cancer cells and in drug resistance. [less ▲]

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See detailnFactors : un logiciel pour déterminer le nombre de facteurs à retenir dans une analyse factorielle exploratoire
Raîche, Gilles; Magis, David ULg

Scientific conference (2009, October)

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See detailNFKBIA Deletion in Glioblastomas.
Bredel, M.; Scholtens, D. M.; Yadav, A. K. et al

in New England Journal of Medicine [=NEJM] (2011)

Background Amplification and activating mutations of the epidermal growth factor receptor (EGFR) oncogene are molecular hallmarks of glioblastomas. We hypothesized that deletion of NFKBIA (encoding ... [more ▼]

Background Amplification and activating mutations of the epidermal growth factor receptor (EGFR) oncogene are molecular hallmarks of glioblastomas. We hypothesized that deletion of NFKBIA (encoding nuclear factor of kappa-light polypeptide gene enhancer in B-cells inhibitor-alpha), an inhibitor of the EGFR-signaling pathway, promotes tumorigenesis in glioblastomas that do not have alterations of EGFR. Methods We analyzed 790 human glioblastomas for deletions, mutations, or expression of NFKBIA and EGFR. We studied the tumor-suppressor activity of NFKBIA in tumor-cell culture. We compared the molecular results with the outcome of glioblastoma in 570 affected persons. Results NFKBIA is often deleted but not mutated in glioblastomas; most deletions occur in nonclassical subtypes of the disease. Deletion of NFKBIA and amplification of EGFR show a pattern of mutual exclusivity. Restoration of the expression of NFKBIA attenuated the malignant phenotype and increased the vulnerability to chemotherapy of cells cultured from tumors with NFKBIA deletion; it also reduced the viability of cells with EGFR amplification but not of cells with normal gene dosages of both NFKBIA and EGFR. Deletion and low expression of NFKBIA were associated with unfavorable outcomes. Patients who had tumors with NFKBIA deletion had outcomes that were similar to those in patients with tumors harboring EGFR amplification. These outcomes were poor as compared with the outcomes in patients with tumors that had normal gene dosages of NFKBIA and EGFR. A two-gene model that was based on expression of NFKBIA and O(6)-methylguanine DNA methyltransferase was strongly associated with the clinical course of the disease. Conclusions Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. [less ▲]

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See detailNG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury.
Buss, Armin; Pech, Katrin; Kakulas, Byron A et al

in BMC Neurology (2009), 9

BACKGROUND: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has ... [more ▼]

BACKGROUND: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has demonstrated rapid re-expression of CSPGs at and around the lesion site. The pharmacological digestion of CSPGs in such lesion models results in substantially enhanced axonal regeneration and a significant functional recovery. The potential therapeutic relevance of interfering with CSPG expression or function following experimental injuries seems clear, however, the spatio-temporal pattern of expression of individual members of the CSPG family following human spinal cord injury is only poorly defined. In the present correlative investigation, the expression pattern of CSPG family members NG2, neurocan, versican and phosphacan was studied in the human spinal cord. METHODS: An immunohistochemical investigation in post mortem samples of control and lesioned human spinal cords was performed. All patients with traumatic SCI had been clinically diagnosed as having "complete" injuries and presented lesions of the maceration type. RESULTS: In sections from control spinal cord, NG2 immunoreactivity was restricted to stellate-shaped cells corresponding to oligodendrocyte precursor cells. The distribution patterns of phosphacan, neurocan and versican in control human spinal cord parenchyma were similar, with a fine reticular pattern being observed in white matter (but also located in gray matter for phosphacan). Neurocan staining was also associated with blood vessel walls. Furthermore, phosphacan, neurocan and versican were present in the myelin sheaths of ventral and dorsal nerve roots axons. After human SCI, NG2 and phosphacan were both detected in the evolving astroglial scar. Neurocan and versican were detected exclusively in the lesion epicentre, being associated with infiltrating Schwann cells in the myelin sheaths of invading peripheral nerve fibres from lesioned dorsal roots. CONCLUSION: NG2 and phosphacan were both present in the evolving astroglial scar and, therefore, might play an important role in the blockade of successful CNS regeneration. Neurocan and versican, however, were located at the lesion epicentre, associated with Schwann cell myelin on regenerating peripheral nerve fibres, a distribution that was unlikely to contribute to failed CNS axon regeneration. The present data points to the importance of such correlative investigations for demonstrating the clinical relevance of experimental data. [less ▲]

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See detailNG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in the postnatal hippocampus
Aguirre, Adan A.; Chittajallu, Ramesh; Belachew, Shibeshih ULg et al

in Journal of Cell Biology (2004), 165(4), 575-589

The subventricular zone (SVZ) is a source of neural progenitors throughout brain development. The identification and purification of these progenitors and the analysis of their lineage potential are ... [more ▼]

The subventricular zone (SVZ) is a source of neural progenitors throughout brain development. The identification and purification of these progenitors and the analysis of their lineage potential are fundamental issues for future brain repair therapies. We demonstrate that early postnatal NG2-expressing (NG2(+)) progenitor cells located in the SVZ self-renew in vitro and display phenotypic features of transit-amplifier type C-like multipotent cells. NG2(+) cells in the SVZ are highly proliferative and express the epidermal growth factor receptor, the transcription factors Dlx, Mash1, and Olig2, and the Lewis X (LeX) antigen. We show that grafted early postnatal NG2(+) cells generate hippocampal GABAergic interneurons that propagate action potentials and receive functional glutamatergic synaptic inputs. Our work identifies Dlx(+)/Mash1(+)/LeX(+)/NG2(+)/GFAP-negative cells of the SVZ as a new class of postnatal multipotent progenitor cells that may represent a specific cellular reservoir for renewal of postnatal and adult inhibitory interneurons in the hippocampus. [less ▲]

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See detailNGAL biomarqueur de lésion rénale
Gagneux-Brunon, Amandine; DELANAYE, Pierre ULg; LEGRAND, Delphine ULg et al

in Néphrologie & Thérapeutique (2012), 8(7), 508-515

Le diagnostic precoce de l’insufissance renale aigue (IRA) est necessaire et devrait se faire au stade de lesion renale avant meme la degradation du debit de filtration glomerulaire. Plusieurs ... [more ▼]

Le diagnostic precoce de l’insufissance renale aigue (IRA) est necessaire et devrait se faire au stade de lesion renale avant meme la degradation du debit de filtration glomerulaire. Plusieurs biomarqueurs d’atteinte renale aigue sont actuellement a l’etude. Parmi ceux-ci, le Neutrophil Gelatinase Associated Lipocalin (NGAL) semble l’un des plus prometteurs et fait l’objet de nombreuses publications. La performance diagnostique de NGAL, dose dans le plasma ou les urines, pour le depistage de l’IRA depend de nombreux facteurs. Bien que les donnees experimentales recentes soient en faveur de l’utilisation preferentielle du dosage urinaire de NGAL, les donnees cliniques issues de nombreuses etudes ne permettent pas de trancher formellement sur la superiorite du dosage urinaire par rapport au dosage plasmatique pour le depistage des atteintes renales aigues. Il n’en reste pas moins que sur le plan analytique, les techniques de dosage du NGAL urinaire sont actuellement plus fiables que celles du dosage plasmatique. La performance diagnostique de NGAL dans un contexte d’IRA est maximale en chirurgie cardiaque pediatrique. Les resultats, chez l’adulte en postoperatoire de chirurgie cardiaque et dans d’autres situations (reanimation, urgences, transplantation), sont moins convaincants. Par ailleurs, il n’est actuellement pas possible d’extrapoler des etudes cliniques une valeur seuil discriminante unique de NGAL, aussi bien dans les urines que dans le plasma. D’autres etudes sont necessaires pour valider definitivement NGAL comme biomarqueur de l’atteinte renale aigue et en preciser les conditions d’utilisation en pratique clinique. [less ▲]

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