References of "Birembaut, P"
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See detailControl of CXCL8/IL-8 expression by ZO-1:
Lesage, J; Suarez-Carmona, Meggy ULg; Grelet, S et al

Poster (2015, October 12)

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See detailThe human NANOS3 gene contributes to lung tumour invasion by inducing epithelial-mesenchymal transition
Grelet, S; Andries, V; Polette, M et al

in Journal of Pathology (The) (2015), 237(1), 25-37

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See detailRegulation of membrane-type 1 matrix metalloproteinase expression by zonula occludens-2 in human lung cancer cells.
Luczka, E.; Syne, Laïdya ULg; Nawrocki-Raby, B. et al

in Clinical & Experimental Metastasis (2013), 30(7), 833-843

During tumor invasion, tumor epithelial cells acquire migratory and invasive properties involving important phenotypic alterations. Among these changes, one can observe reorganization or a loss of cell ... [more ▼]

During tumor invasion, tumor epithelial cells acquire migratory and invasive properties involving important phenotypic alterations. Among these changes, one can observe reorganization or a loss of cell-cell adhesion complexes such as tight junctions (TJs). TJs are composed of transmembrane proteins (occludin, claudins) linked to the actin cytoskeleton through cytoplasmic adaptor molecules including those of the zonula occludens family (ZO-1, -2, -3). We here evaluated the potential role of ZO-2 in the acquisition of invasive properties by tumor cells. In vivo, we showed a decrease of ZO-2 expression in bronchopulmonary cancers, with a preferential localization in the cytoplasm. In addition, in vitro, the localization of ZO-2 varied according to invasive properties of tumor cells, with a cytoplasmic localization correlating with invasion. In addition, we demonstrated that ZO-2 inhibition increases invasive and migrative capacities of invasive tumor cells. This was associated with an increase of MT1-MMP. These results suggest that ZO-2, besides its structural role in tight junction assembly, can act also as a repressor of tumor progression through its ability to reduce the expression of tumor-promoting genes in invasive tumor cells. [less ▲]

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See detailRegulation of CXCL8/IL-8 expression by Zonula Occludens-1 in human breast cancer cells.
Brysse, Anne ULg; Mestdagt, Mélanie ULg; Polette, Myriam et al

in Molecular Cancer Research (2012), 10(1), 121-32

Accumulating data now suggest that ZO-1, once delocalized from tight junctions, could be implicated in the regulation of tumor promoting genes. Because of their major implication in different steps of ... [more ▼]

Accumulating data now suggest that ZO-1, once delocalized from tight junctions, could be implicated in the regulation of tumor promoting genes. Because of their major implication in different steps of tumor progression, we investigated here the influence of ZO-1 on chemokines expression in breast cancer cells. Using GeneArray analysis to compare chemokine mRNA expression in breast tumor cells transfected with a siRNA against ZO-1, we identified CXCL-8/IL-8 as a major potential target of ZO-1 signaling, being strongly downregulated following ZO-1 siRNA transfection. Examining further the relationship between ZO-1 and IL-8, we first demonstrated that CXCL8/IL-8 expression correlates with a relocalization of ZO-1 in several breast cancer cell lines. Moreover, CXCL8/IL-8 is downregulated in invasive BT549 cells transfected with 3 different ZO-1 siRNA and overexpressed in non-invasive BT20 and SKBR3 cells transfected with vectors expressing ZO-1. We also provide evidence for an activation of the CXCL8/IL-8 promoter by ZO-1. Finally, we demonstrate that the regulation of CXCL8/IL-8 by ZO-1 is independent of the beta-catenin pathway. Our results thus clearly demonstrate an implication of ZO-1 in CXCL8/IL-8 regulation. Because of the major implications of CXCL8/IL-8 in tumor invasion, such a regulation could play an important role in breast cancer progression. [less ▲]

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See detailImplication of tight junctions in tumor invasion
Luczka, E.; Nawrocki-Raby, B; Birembaut, P et al

Poster (2011, October 10)

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See detailThe fragile histidine triad gene regulates epithelial-mesenchymal transition associated with invasion of lung tumor cells.
Joannes, A; Bonnomet, Arnaud; Polette, Myriam et al

Poster (2011, October 10)

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See detailFhit regulates invasion of lung tumor cells
Joannes, A.; Bonnomet, A.; Bindels, S. et al

in Oncogene (2010), 29(8), 1203-13

In many types of cancers, the fragile histidine triad (Fhit) gene is frequently targeted by genomic alterations leading to a decrease or loss of gene and protein expression. Fhit has been described as a ... [more ▼]

In many types of cancers, the fragile histidine triad (Fhit) gene is frequently targeted by genomic alterations leading to a decrease or loss of gene and protein expression. Fhit has been described as a tumor suppressor gene because of its ability to induce apoptosis and to inhibit proliferation of tumor cells. Moreover, several studies have shown a correlation between the lack of Fhit expression and tumor aggressiveness, thus suggesting that Fhit could be involved in tumor progression. In this study, we explored the potential role of Fhit during tumor cell invasion. We first showed that a low Fhit expression is associated with in vivo and in vitro invasiveness of tumor cells. Then, we showed that Fhit overexpression in Fhit-negative highly invasive NCI-H1299 cells by transfection of Fhit cDNA and Fhit inhibition in Fhit-positive poorly invasive HBE4-E6/E7 cells by transfection of Fhit small interfering RNA induce, respectively, a decrease and an increase in migratory/invasive capacities. These changes in cell behavior were associated with a reorganization of tight and adherens junction molecules and a regulation of matrix metalloproteinase and vimentin expression. These results show that Fhit controls the invasive phenotype of lung tumor cells by regulating the expression of genes associated with epithelial–mesenchymal transition. [less ▲]

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See detailRegulation of CXCL8/IL-8 expression by Zonula Occludens-1 in human breast cancer cells.
Mestdagt, M; Polette, M; Bindels, S et al

Poster (2009, April 18)

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See detailThe E-cadherin-repressed hNanos1 gene induces tumor cell invasion by upregulating MT1-MMP expression
Bonnomet, A.; Polette, M.; Strumane, K. et al

in Oncogene (2008), 27(26), 3692-9

In this study, we examined the role of the E-cadherin-repressed gene human Nanos1 (hNanos1) in tumor invasion process. First, our in vivo study revealed that hNanos1 mRNAs were overexpressed in invasive ... [more ▼]

In this study, we examined the role of the E-cadherin-repressed gene human Nanos1 (hNanos1) in tumor invasion process. First, our in vivo study revealed that hNanos1 mRNAs were overexpressed in invasive lung carcinomas. Moreover, hNanos1 was co-localized with MT1-MMP (membrane type 1-matrix metalloproteinase) in E-cadherin-negative invasive lung tumor clusters. Using an inducible Tet-on system, we showed that induction of hNanos1 expression in DLD1 cells increased their migratory and invasive abilities in a three-dimensional migration and in a modified Boyden chamber assay. Accordingly, we demonstrated that hNanos1 upregulated MT1-MMP expression at the mRNA and protein levels. Inversely, using an RNA interference strategy to inhibit hNanos1 expression in invasive Hs578T, BT549 and BZR cancer cells, we observed a downregulation of MT1-MMP mRNA and protein and concomitantly a decrease of the invasive capacities of tumor cells in a modified Boyden chamber assay. Taken together, our results demonstrate that hNanos1, by regulating MT1-MMP expression, plays an important role in the acquisition of invasive properties by epithelial tumor cells. [less ▲]

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See detailRegulation of CXCL8/IL-8 by Zonula Occludens-1 during breast tumor-associated epithelial-to-mesenchymal transitions.
Mestdagt, M; Polette, M; Bindels, S et al

Poster (2007, December 05)

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See detailRegulation of CXCL8/IL-8 by Zonula Occludens-1 during breast tumor-associated epithelial-to-mesenchymal transitions.
Mestdagt, M; Polette, M; Bindels, S et al

Poster (2007, September 10)

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See detailbeta-Catenin and ZO-1: Shuttle molecules involved in tumor invasion-associated epithelial-mesenchymal transition processes
Polette, M.; Mestdagt, Mélanie ULg; Bindels, Sandrine ULg et al

in Cells Tissues Organs (2007), 185(1-3), 61-65

The cytoplasmic/nuclear relocalization of beta-catenin and ZO-1 from the adherens and tight junctions are common processes of the epithelial-mesenchymal transition (EMT) associated with tumor invasion ... [more ▼]

The cytoplasmic/nuclear relocalization of beta-catenin and ZO-1 from the adherens and tight junctions are common processes of the epithelial-mesenchymal transition (EMT) associated with tumor invasion. Data are now accumulating to demonstrate that these molecules, which shuttle between the plasma membrane and the nucleus or the cytosol, are involved in signaling pathways, and contribute to the regulation of genes such as vimentin or matrix metalloproteinase-14 which are turned on during EMT. Copyright (c) 2007 S. Karger AG, Basel. [less ▲]

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See detailExpression of a disintegrin and metalloprotease (ADAM and ADAMTS) enzymes in human non-small-cell lung carcinomas (NSCLC)
Rocks, Natacha ULg; Paulissen, Geneviève ULg; Quesada Calvo, Florence ULg et al

in British Journal of Cancer (2006), 94(5), 724-730

A Disintegrin and Metalloprotease (ADAM) are transmembrane proteases displaying multiple functions. ADAM with ThromboSpondin-like motifs (ADAMTS) are secreted proteases characterised by thrombospondin (TS ... [more ▼]

A Disintegrin and Metalloprotease (ADAM) are transmembrane proteases displaying multiple functions. ADAM with ThromboSpondin-like motifs (ADAMTS) are secreted proteases characterised by thrombospondin (TS) motifs in their C-terminal domain. The aim of this work was to evaluate the expression pattern of ADAMs and ADAMTS in non small cell lung carcinomas (NSCLC) and to investigate the possible correlation between their expression and cancer progression. Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunohistochemical analyses were performed on NSCLC samples and corresponding nondiseased tissue fragments. Among the ADAMs evaluated (ADAM-8, -9, -10, -12, -15, -17, ADAMTS-1, TS-2 and TS-12), a modulation of ADAM-12 and ADAMTS-1 mRNA expression was observed. Amounts of ADAM-12 mRNA transcripts were increased in tumour tissues as compared to the corresponding controls. In sharp contrast, ADAMTS-1 mRNA levels were significantly lower in tumour tissues when compared to corresponding nondiseased lung. These results were corroborated at the protein level by Western blot and immunohistochemistry. A positive correlation was observed between the mRNA levels of ADAM-12 and those of two vascular endothelial growth factor (VEGF)-A isoforms (VEGF-A(165) and VEGF-A(121)). Taken together, these results providing evidence for an overexpression of ADAM-12 and a lower expression of ADAMTS-1 in non-small-cell lung cancer suggest that these proteases play different functions in cancer progression. [less ▲]

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See detailMembrane-type 1 matrix metalloproteinase expression is regulated by zonula occludens-1 in human breast cancer cells
Polette, M.; Gilles, Christine ULg; Nawrocki-Raby, B. et al

in Cancer Research (2005), 65(17), 7691-7698

The acquisition of a migratory/invasive phenotype by tumor cells is characterized by the loss of cell-cell adhesion contacts and the expression of degradative properties. In this study, we examined the ... [more ▼]

The acquisition of a migratory/invasive phenotype by tumor cells is characterized by the loss of cell-cell adhesion contacts and the expression of degradative properties. In this study, we examined the effect of the disorganization of occludin/zomda occludens (ZO)-1 tight junction (TJ) complexes on the expression of membrane-type I matrix metalloproteinase (MT1-MMP). We first compared the expression of MT1-MMP and the localization of occludin/ZO-1 complexes in breast tumor cell lines displaying various degrees of invasiveness. We showed that the expression of MT1-MMP in invasive breast tumor cell lines correlates with the absence of occludin and with a cytoplasmic localization of ZO-1. In contrast, noninvasive cell lines displayed a membrane staining for both ZO-1 and occludin and did not express MT1-MMP. In vivo, cytoplasmic ZO-1 and MTI-MMP could be detected in invasive tumor clusters of human breast carcinomas. We then used RNA interference strategy to inhibit ZO-1 expression in invasive BT549 cells and to evaluate the effect of ZO-1 downregulation on MTI-MMP expression. We observed that ZO-1 small interfering RNA transfection down-regulates MT1-MMP mRNAs and proteins and subsequently decreases the ability of tumor cells to invade a reconstituted basement membrane in a Boyden chamber assay. Inversely, transfection of expression vectors encoding wild-type ZO-1 or the NH2-terminal fragment of ZO-1 comprising the PSD95/DLG/ZO-1 domains in BT549 activated a human MT1-MMP promoter luciferase reporter construct and increased cell invasiveness. Such transfections concomitantly activated the beta-catenin/TCF/LEF pathway. Our results therefore show that ZO-1, besides its structural role in TJ assembly, can intervene in signaling events promoting tumor cell invasion. [less ▲]

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See detailTumor invasion and matrix metalloproteinases
Polette, M.; Nawrocki-Raby, B.; Gilles, Christine ULg et al

in Critical Reviews in Oncology/Hematology (2004), 49(3), 179-86

Matrix metalloproteinases (MMPs) are proteolytic enzymes which play a major role in tumour invasion. They are mainly produced by host stromal cells in most carcinomas and their expression implies a close ... [more ▼]

Matrix metalloproteinases (MMPs) are proteolytic enzymes which play a major role in tumour invasion. They are mainly produced by host stromal cells in most carcinomas and their expression implies a close co-operation between tumour and stromal cells. Increasing data also demonstrate that, in association with a process of epithelial-to-mesenchymal transition, many MMPs can be expressed by tumour cell themselves. Their most well-known role is the degradation of extra-cellular matrix macromolecules which in turn may regulate tumour invasion in some conditions. This ECM degradation generates some matrikins which are also implicated in tumour invasion and angiogenesis. Moreover, MMPs are also implicated in the degradation of cell adhesion molecules and release and activation of growth factors. [less ▲]

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See detailInvasion and metastatis: defining the invasive and migratory phenotype
Gilles, Christine ULg; Polette, M; Mestdagt, M et al

Conference (2003, October 15)

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See detailDisorganization of cell-cell junctions regulates vimentin expression during tumor invasion-associated EMT.
Gilles, Christine ULg; Polette, M; Mestadgt, M et al

Conference (2003, October 05)

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See detailE-cadherin mediates MMP down-regulation in highly invasive bronchial tumor cells
Nawrocki-Raby, B.; Gilles, Christine ULg; Polette, M. et al

in American Journal of Pathology (2003), 163(2), 653-661

The disorganization of E-cadherin/catenin complexes and the overexpression of matrix metalloproteinases (MMPs) are frequently involved in the capacity of epithelial cells to acquire an invasive phenotype ... [more ▼]

The disorganization of E-cadherin/catenin complexes and the overexpression of matrix metalloproteinases (MMPs) are frequently involved in the capacity of epithelial cells to acquire an invasive phenotype. The functional link between F-cadherin and MMPs was studied by transfecting invasive bronchial BZR tumor cells with human E-cadherin cDNA. Using different in vitro (cell dispersion, modified Boyden chamber) and in vivo assays (human airway epithelial xenograft), we showed that E-cadherin-positive clones displayed a decrease of invasive abilities. As shown by immunoprecipitation, the re-expressed E-cadherin was able to sequestrate one part of free cytoplasmic beta-catenin in BZR cells. The decrease of beta-catenin transcriptional activity in E-cadherin-transfected clones was demonstrated using the TOP-FLASH reporter construct. Finally, we observed a decrease of MMP-1, MMP-3, MMP-9, and MT1-MMP, both at the mRNA and at the protein levels, in E-cadherin-positive clones whereas no changes in MMP-2, TIMP-1, or TIMP-2 were observed when compared with control clones. Moreover, zymography analysis revealed a loss of MMP-2 activation ability in E-cadherin-positive clones treated with the concanavalin A lectin. These data demonstrate a direct role of E-cadherin/catenin complex organization in the regulation of MMPs and suggest an implication of this regulation in the expression of an invasive phenotype by bronchial tumor cells. [less ▲]

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See detailUpregulation of MMPs by soluble E-cadherin in human lung tumor cells
Nawrocki-Raby, B.; Gilles, Christine ULg; Polette, M. et al

in International Journal of Cancer = Journal International du Cancer (2003), 105(6), 790-795

Loss of E-cadherin/catenin mediated cell-cell adhesion and overexpression of matrix metalloproteinases (MMPs) are largely involved in tumor invasion. It has been recently shown that high levels of a ... [more ▼]

Loss of E-cadherin/catenin mediated cell-cell adhesion and overexpression of matrix metalloproteinases (MMPs) are largely involved in tumor invasion. It has been recently shown that high levels of a soluble 80 kDa fragment of E-cadherin, resulting from a cleavage by IVIMPs, are found in serum and in urine from cancer patients. Additionally, this soluble E-cadherin (sE-CAD) promotes cell invasion into chick heart and into collagen type I gels. The aim of our study was to examine the mechanism of sE-CAD-induced cell invasion. Since MMPs play a crucial role in invasion, we looked for induction of MMPs by sE-CAD in noninvasive human lung tumor cells 16HBE. An induction of MMP-2, MMP-9 and MTI-MMP expression was observed both at the mRNA and at the protein level in the presence of sE-CAD (in conditioned medium form or in E-cadherin HAV peptide form). No induction of MMP-I, -3 and -7 or variation of the levels of their inhibitors, TIMP-I and TIMP-2, were detected. The biologic relevance of the sE-CAD-induced MMP upregulation was tested by demonstrating that sE-CAD promotes in vitro cell invasion in a modified Boyden chamber assay. These data provide new insight into mechanisms of tumor invasion by ectodomain shedding of the cell-cell adhesion molecule E-cadherin. (C) 2003 Wiley-Liss, Inc. [less ▲]

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See detailTransactivation of vimentin by beta-catenin in human breast cancer cells
Gilles, Christine ULg; Polette, M.; Mestdagt, Mélanie ULg et al

in Cancer Research (2003), 63(10), 2658-2664

The cytoplasmic and nuclear redistribution of beta-catenin and the de novo expression of vimentin are frequently involved in the epithelial-to-mesenchymal transition associated with increased invasive ... [more ▼]

The cytoplasmic and nuclear redistribution of beta-catenin and the de novo expression of vimentin are frequently involved in the epithelial-to-mesenchymal transition associated with increased invasive/migratory properties of epithelial cells. Because beta-catenin can act as a coactivator of transcription through its binding to the T-cell factor (TCF)/lymphoid enhancer factor 1 transcription factor family, we have explored the possibility that beta-catenin/TCF could directly transactivate vimentin. We first compared vimentin expression in relation with the localization of beta-catenin in eight breast cancer cell lines displaying various degrees of invasiveness and in a model of cell migration using human mammary MCF10A cells. We could thus show a cytoplasmic and/or nuclear distribution of beta-catenin in invasive/migratory cells expressing vimentin, but not in noninvasive/stationary vimentin-negative cell lines. In addition, the human vimentin promoter was found to be up-regulated by beta-catenin and TCF-4 cotransfection. Varying with the cellular background, a diminution of this up-regulation was observed when the putative beta-catenin/TCF binding site of the vimentin promoter was mutated. Our results therefore demonstrate that the vimentin promoter is a target of the beta-catenin/TCF pathway and strongly suggest an implication of this regulation in epithelial cell migration/invasion. [less ▲]

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