16 results on '"de Wever, Olivier"'
Search Results
2. Cell motility and breast cancer metastasis
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Bracke, Marc E., De Maeseneer, Daan, Van Marck, Veerle, Derycke, Lara, Vanhoecke, Barbara, De Wever, Olivier, Depypere, Herman T., Ablin, Richard J., editor, Jiang, Wen G., editor, Mansel, Robert E., editor, and Fodstad, Oystein, editor
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- 2007
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3. Robust sequential biophysical fractionation of blood plasma to study variations in the biomolecular landscape of systemically circulating extracellular vesicles across clinical conditions.
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Vergauwen, Glenn, Tulkens, Joeri, Pinheiro, Cláudio, Avila Cobos, Francisco, Dedeyne, Sándor, De Scheerder, Marie‐Angélique, Vandekerckhove, Linos, Impens, Francis, Miinalainen, Ilkka, Braems, Geert, Gevaert, Kris, Mestdagh, Pieter, Vandesompele, Jo, Denys, Hannelore, De Wever, Olivier, and Hendrix, An
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EXTRACELLULAR vesicles ,BLOOD plasma ,DENSITY gradient centrifugation ,BREAST cancer ,NON-coding RNA ,BLOOD testing - Abstract
Separating extracellular vesicles (EV) from blood plasma is challenging and complicates their biological understanding and biomarker development. In this study, we fractionate blood plasma by combining size‐exclusion chromatography (SEC) and OptiPrep density gradient centrifugation to study clinical context‐dependent and time‐dependent variations in the biomolecular landscape of systemically circulating EV. Using pooled blood plasma samples from breast cancer patients, we first demonstrate the technical repeatability of blood plasma fractionation. Using serial blood plasma samples from HIV and ovarian cancer patients (n = 10) we next show that EV carry a clinical context‐dependent and/or time‐dependent protein and small RNA composition, including miRNA and tRNA. In addition, differential analysis of blood plasma fractions provides a catalogue of putative proteins not associated with systemically circulating EV. In conclusion, the implementation of blood plasma fractionation allows to advance the biological understanding and biomarker development of systemically circulating EV. [ABSTRACT FROM AUTHOR]
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- 2021
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4. Adipose tissue in breast cancer : not an idle bystander but an active participant in breast cancer progression
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Lapeire, Lore, Hendrix, An, Lambein, Kathleen, Braems, Geert, Valet, P, Van den Broecke, Rudy, Bracke, Marc, Cocquyt, Veronique, Denys, Hannelore, and De Wever, Olivier
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obesity ,breast cancer ,Medicine and Health Sciences ,skin and connective tissue diseases ,adipokines ,adipose tissue - Abstract
Background: Adipose tissue is a dynamic organ that secretes a plethora of molecules called adipokines. In breast cancer we find a unique situation were genetically changed cells (the cancer cells) are in close contact with adipocytes. Moreover, obesity is a known negative prognostic marker for postmenopausal breast cancer patients. We hypothesize that adipocyte-derived factors influence breast cancer progression. Materials and methods: Adipose tissue was collected from breast cancer patients undergoing a mastectomy. After macroscopic removal of blood vessels and connective tissue, the adipose tissue was carefully cut into 2-3mm3 pieces and were incubated in specific adipose-tissue culture medium. After 24h, the medium was collected and the quality was checked by determining the concentration of total proteins, leptin, adiponectin, TNFalpha and triglycerides. This conditioned medium of adipose tissue (CM AT) was used for in vitro experimentation with MCF-7 breast cancer cells. Results: Effect of AT on morphology and aggregation: when MCF-7 cells are grown in a culture flask, they tend to form round compact islands. Under influence of CM AT, the islands form sharp edges, the cells in an island can be counted individually and they show scattering. Importantly, despite the major changes in cellular morphology, CM AT removal rescued the compact island formation of MCF-7 cells. In the slow aggregation assay, cells treated with CM AT (and a subtherapeutic concentration of a neutralizing E-cadherin antibody) lost the ability to form compact aggregates. Furthermore, MCF-7 spheroids placed inside adipose tissue showed massive reorganization into an irregularly shaped mass. Effect of AT on proliferation: starting from an equal number of cells and counting them every 2 days, it became clear that MCF-7 cells with CM AT had a higher rate of proliferation than MCF-7 cells in control medium. This stimulation of proliferation was confirmed by cell cycle analysis which revealed a doubling of cells in the G2/M phase, and western blot which showed an upregulation of cyclin A and cyclin E, both positive regulators of the cell cycle. Effect of AT on invasion: a 24h collagen type I invasion assay revealed invasive characteristics of MCF-7 cells treated with CM AT while MCF-7 cells in control conditions are round and non-invasive. In contrast, a transwell collagen test over 14 days was not able to show MCF-7 cells invading the collagen gel under influence of CM AT. However, the growth pattern of MCF-7 cells on the collagen gel was clearly disorganised when compared with the control situation. Conclusion: These findings suggest that adipose tissue-derived factors exert a dramatic selective force on patterning, invasion and growth of MCF-7 breast cancer cells. Unraveling the mechanism behind these observations may provide vital information regarding the link between obesity and poor prognosis in postmenopausal breast cancer.
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- 2011
5. When fat becomes an ally of the enemy: adipose tissue as collaborator in human breast cancer.
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Lapeire, Lore, Denys, Hannelore, Cocquyt, Véronique, and De Wever, Olivier
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FAT ,ADIPOSE tissues ,BREAST cancer ,LEPTIN ,OBESITY - Abstract
Since the discovery of leptin in 1994, our vision of adipose tissue as a static organ regulating mainly lipid storage and release has been completely overthrown, and adipose tissue is now seen as an active and integral organ in human physiology. In the past years, extensive research has tremendously given us more insights in the mechanisms and pathways involved not only in normal but also in 'sick' adipose tissue, for example, in obesity and lipodystrophy. With growing evidence of a link between obesity and several types of cancer, research focusing on the interaction between adipose tissue and cancer has begun to unravel the interesting but complex multi-lateral communication between the different players. With breast cancer as one of the first cancer types where a positive correlation between obesity and breast cancer incidence and prognosis in post-menopausal women was found, we have focused this review on the paracrine and endocrine role of adipose tissue in breast cancer initiation and progression. As important inter-species differences in adipose tissue occur, we mainly selected human adipose tissue and breast cancer-based studies with a short reflection on therapeutic possibilities. This review is part of the special issue on "Adiposopathy in Cancer and (Cardio)Metabolic Diseases". [ABSTRACT FROM AUTHOR]
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- 2015
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6. The Quorum Sensing Peptides PhrG, CSP and EDF Promote Angiogenesis and Invasion of Breast Cancer Cells In Vitro.
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De Spiegeleer, Bart, Verbeke, Frederick, D’Hondt, Matthias, Hendrix, An, Van De Wiele, Christophe, Burvenich, Christian, Peremans, Kathelijne, De Wever, Olivier, Bracke, Marc, and Wynendaele, Evelien
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BREAST cancer ,QUORUM sensing ,PEPTIDES ,CANCER cells ,CHORIOALLANTOIS ,NEOVASCULARIZATION - Abstract
The role of the human microbiome on cancer progression remains unclear. Therefore, in this study, we investigated the influence of some quorum sensing peptides, produced by diverse commensal or pathogenic bacteria, on breast cancer cell invasion and thus cancer outcome. Based on microscopy, transcriptome and Chick Chorioallantoic Membrane (CAM) analyses, four peptides (PhrG from B. subtilis, CSP from S. mitis and EDF from E. coli, together with its tripeptide analogue) were found to promote tumour cell invasion and angiogenesis, thereby potentially influencing tumour metastasis. Our results offer not only new insights on the possible role of the microbiome, but also further opportunities in cancer prevention and therapy by competing with these endogenous molecules and/or by modifying people’s life style. [ABSTRACT FROM AUTHOR]
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- 2015
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7. A nanobody targeting the F-actin capping protein CapG restrains breast cancer metastasis.
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Van Impe, Katrien, Bethuyne, Jonas, Cool, Steven, Impens, Francis, Ruano-Gallego, David, De Wever, Olivier, Vanloo, Berlinda, Van Troys, Marleen, Lambein, Kathleen, Boucherie, Ciska, Martens, Evelien, Zwaenepoel, Olivier, Hassanzadeh-Ghassabeh, Gholamreza, Vandekerckhove, Joël, Gevaert, Kris, Fernández, Luis Ángel, Sanders, Niek N., and Gettemans, Jan
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BREAST cancer ,F-actin ,CAPPING proteins ,CYTOSKELETON ,GENE expression ,CANCER cells - Abstract
Introduction Aberrant turnover of the actin cytoskeleton is intimately associated with cancer cell migration and invasion. Frequently however, evidence is circumstantial and a reliable assessment of the therapeutic significance of a gene product is offset by lack of inhibitors that target biological properties of a protein, as most conventional drugs do, instead of the corresponding gene. Proteomic studies have demonstrated over-expression of CapG, a constituent of the actin cytoskeleton, in breast cancer. Indirect evidence suggests that CapG is involved in tumor cell dissemination and metastasis. In this study, we used llama-derived CapG single domain antibodies or nanobodies in a breast cancer metastasis model to address if inhibition of CapG activity holds therapeutic merit. Methods We raised single domain antibodies (nanobodies) against human CapG and used these as intrabodies (immunomodulation) following lentiviral transduction of breast cancer cells. Functional characterization of nanobodies was performed to identify which biochemical properties of CapG are perturbed. Orthotopic and tail vein in vivo models of metastasis in nude mice were used to assess cancer cell spreading. Results Using G-actin and F-actin binding assays we identified a CapG nanobody that binds with nanomolar affinity to the first CapG domain. Consequently, CapG interaction with actin monomers or actin filaments is blocked. Intracellular delocalization experiments demonstrated that the nanobody interacts with CapG in the cytoplasmic environment. Expression of the nanobody in breast cancer cells restrained cell migration and Matrigel® invasion. Notably, the nanobody prevented formation of lung metastatic lesions in orthotopic xenograft and tail vein models of metastasis in immunodeficient mice. We show that CapG nanobodies can be delivered into cancer cells using bacteria harboring a type III protein secretion system (T3SS). Conclusions CapG inhibition strongly reduces breast cancer metastasis. A nanobody-based approach offers a fast track for gauging the therapeutic merit of drug targets. Mapping of the nanobody-CapG interface may provide a platform for rational design of pharmacological compounds. [ABSTRACT FROM AUTHOR]
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- 2013
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8. Comparative Analysis of Dynamic Cell Viability, Migration and Invasion Assessments by Novel Real-Time Technology and Classic Endpoint Assays.
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Limame, Ridha, Wouters, An, Pauwels, Bea, Fransen, Erik, Peeters, Marc, Lardon, Filip, De Wever, Olivier, and Pauwels, Patrick
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CELL migration ,CELL motility ,CELL proliferation ,CELL-mediated cytotoxicity ,CANCER cells ,BREAST cancer ,LUNG cancer - Abstract
Background: Cell viability and motility comprise ubiquitous mechanisms involved in a variety of (patho)biological processes including cancer. We report a technical comparative analysis of the novel impedance-based xCELLigence Real-Time Cell Analysis detection platform, with conventional label-based endpoint methods, hereby indicating performance characteristics and correlating dynamic observations of cell proliferation, cytotoxicity, migration and invasion on cancer cells in highly standardized experimental conditions. Methodology/Principal Findings: Dynamic high-resolution assessments of proliferation, cytotoxicity and migration were performed using xCELLigence technology on the MDA-MB-231 (breast cancer) and A549 (lung cancer) cell lines. Proliferation kinetics were compared with the Sulforhodamine B (SRB) assay in a series of four cell concentrations, yielding fair to good correlations (Spearman's Rho 0.688 to 0.964). Cytotoxic action by paclitaxel (0--100 nM) correlated well with SRB (Rho>0.95) with similar IC
50 values. Reference cell migration experiments were performed using Transwell plates and correlated by pixel area calculation of crystal violet-stained membranes (Rho 0.90) and optical density (OD) measurement of extracted dye (Rho>0.95). Invasion was observed on MDA-MB-231 cells alone using Matrigel-coated Transwells as standard reference method and correlated by OD reading for two Matrigel densities (Rho>0.95). Variance component analysis revealed increased variances associated with impedance-based detection of migration and invasion, potentially caused by the sensitive nature of this method. Conclusions/Significance: The xCELLigence RTCA technology provides an accurate platform for non-invasive detection of cell viability and motility. The strong correlations with conventional methods imply a similar observation of cell behavior and interchangeability with other systems, illustrated by the highly correlating kinetic invasion profiles on different platforms applying only adapted matrix surface densities. The increased sensitivity however implies standardized experimental conditions to minimize technical-induced variance. [ABSTRACT FROM AUTHOR]- Published
- 2012
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9. The role of non-muscle myosin IIA in aggregation and invasion of human MCF-7 breast cancer cells.
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Derycke, Lara, Stove, Christophe, Vercoutter-Edouart, Anne-Sophie, De Wever, Olivier, Dollé, Laurent, Colpaert, Nathalie, Depypere, Herman, Michalski, Jean-Claude, and Bracke, Marc
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MYOSIN ,BREAST cancer ,CELLULAR signal transduction ,CANCER invasiveness ,BLEBBISTATIN ,CADHERINS ,CELL aggregation - Abstract
Human MCF-7/6 breast cancer cells differ from their MCF-7/AZ counterparts by their invasiveness in a number of assays in vitro, such as invasion of MCF-7 spheroids into embryonic chick heart fragments or type I collagen gels. Comparative proteomic analysis of these two variants revealed an identical pattern, except for a 230 kDa protein present in the invasive MCF-7/6 variant, but hardly detectable in the non-invasive MCF-7/AZ one. This protein appeared to be the non-muscle myosin IIA heavy chain (NMIIA), also coined MYH9. Experimental inhibition of NMIIA by reducing either its expression (via stable shRNA transduction) or its function (via the specific ATPase inhibitor blebbistatin) underpinned the decisive role of NMIIA in MCF-7 cell invasion. Inhibition of NMIIA indeed blocked the invasion of MCF-7/6 cells in three-dimensional invasion substrata such as embryonic chick heart fragments and type I collagen gels. Invasiveness of MCF-7/6 cells has been related to poor formation and compaction of aggregates, due to a functionally defective E-cadherin/catenin complex. Both genetic and pharmacological inhibition of NMIIA stimulated MCF-7/6 cell aggregation. Together, these data indicate that NMIIA is a decisive protein for MCF-7 cells to invade, indicating that this molecule is a candidate for targeted anti-invasive treatment. [ABSTRACT FROM AUTHOR]
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- 2011
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10. Effect of the Secretory Small GTPase Rab27B on Breast Cancer Growth, Invasion, and Metastasis.
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Hendrix, An, Maynard, Dawn, Pauwels, Patrick, Braems, Geert, Denys, Hannelore, Broecke, Rudy Van den, Lambert, Jo, Belle, Simon Van, Cocquyt, Veronique, Gespach, Christian, Bracke, Marc, Seabra, Miguel C., Gahl, William A., De Wever, Olivier, and Westbroek, Wendy
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GUANOSINE triphosphatase ,TUMOR suppressor proteins ,EXOCYTOSIS ,BREAST cancer ,CANCER cell growth regulation ,GROWTH regulators - Abstract
Background: Secretory GTPases like Rab27B control vesicle exocytosis and deliver critical proinvasive growth regulators into the tumor microenvironment. The expression and role of Rab27B in breast cancer were unknown. [ABSTRACT FROM PUBLISHER]
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- 2010
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11. Developmental and Cancer Research on the Mammary Gland Nowadays.
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Bracke, Marc and De Wever, Olivier
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MAMMARY glands ,BREAST cancer ,STEM cells ,CELL differentiation ,FLOW cytometry ,METASTASIS ,FIBROBLASTS - Published
- 2011
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12. CCN5, a Novel Transcriptional Repressor of the Transforming Growth Factor β Signaling Pathway.
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Sabbah, Michèle, Prunier, Céline, Ferrand, Nathalie, Megalophonos, Virginie, Lambein, Kathleen, De Wever, Olivier, Nazaret, Nicolas, Lachuer, Joël, Dumont, Sylvie, and Redeuilh, Gérard
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CONNECTIVE tissue growth factor ,NEPHROBLASTOMA ,TRANSFORMING growth factors ,ESTROGEN ,BREAST cancer - Abstract
CCN5 is a member of the CCN (connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed) family and was identified as an estrogen-inducible gene in estrogen receptor-positive cell lines. However, the role of CCN5 in breast carcinogenesis remains unclear. We report here that the CCN5 protein is localized mostly in the cytoplasm and in part in the nucleus of human tumor breast tissue. Using a heterologous transcription assay, we demonstrate that CCN5 can act as a transcriptional repressor presumably through association with histone deacetylase 1 (HDAC1). Microarray gene expression analysis showed that CCN5 represses expression of genes associated with epithelial-mesenchymal transition (EMT) as well as expression of key components of the transforming growth factor β (TGF-β) signaling pathway, prominent among them TGF-βRII receptor. We show that CCN5 is recruited to the TGF-βRII promoter, thereby providing a mechanism by which CCN5 restricts transcription of the TGF-βRII gene. Consistent with this finding, CCN5, we found, functions to suppress TGF-β-induced transcriptional responses and invasion that is concomitant with EMT. Thus, our data uncovered CCN5 as a novel transcriptional repressor that plays an important role in regulating tumor progression functioning, at least in part, by inhibiting the expression of genes involved in the TGF-β signaling cascade that is known to promote EMT. [ABSTRACT FROM AUTHOR]
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- 2011
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13. Role of WISP-2/CCN5 in the Maintenance of a Differentiated and Noninvasive Phenotype in Human Breast Cancer Cells.
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Fritah, Asmaà, Saucier, Cécile, De Wever, Olivier, Bracke, Marc, Bièche, Ivan, Lidereau, Rosette, Gespach, Christian, Drouot, Sylvain, Redeuilh, Gérard, and Sabbah, Michèle
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REGULATION of cell growth ,CELL differentiation ,ESTROGEN ,GROWTH factors ,CONNECTIVE tissues ,MESSENGER RNA ,CANCER cells ,BREAST cancer - Abstract
WISP-2/CCN5 is an estrogen-regulated member of the "connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed" (CCN) family of the cell growth and differentiation regulators. The WISP-2/CCN5 mRNA transcript is undetectable in normal human mammary cells, as well as in highly aggressive breast cancer cell lines, in contrast with its higher level in the breast cancer cell lines characterized by a more differentiated phenotype. We report here that knockdown of WISP-2/CCN5 by RNA interference in estrogen receptor alpha (ERα)-positive MCF-7 breast cancer cells induced an estradiol-independent growth linked to a loss of ERα expression and promoted epithelial-to-mesenchymal transdifferentiation. In contrast, forced expression of WISP-2/CCN5 directed MCF-7 cells toward a more differentiated phenotype. When introduced into the poorly differentiated, estrogen-independent, and invasive MDA-MB-231 breast cancer cells, WISP-2/CCN5 was able to reduce their proliferative and invasive phenotypes. In a series of ERα-positive tumor biopsies, we found a positive correlation between the expression of WISP-2/CCN5 and ID2, a transcriptional regulator of differentiation in normal and transformed breast cells. We propose that WISP-2/CCN5 is an important regulator involved in the maintenance of a differentiated phenotype in breast tumor epithelial cells and may play a role in tumor cell invasion and metastasis. [ABSTRACT FROM AUTHOR]
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- 2008
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14. Stromal integrin α11 regulates PDGFR-β signaling and promotes breast cancer progression.
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Primac, Irina, Maquoi, Erik, Blacher, Silvia, Heljasvaara, Ritva, Van Deun, Jan, Smeland, Hilde Y. H., Canale, Annalisa, Louis, Thomas, Stuhr, Linda, Sounni, Nor Eddine, Cataldo, Didier, Pihlajaniemi, Taina, Pequeux, Christel, De Wever, Olivier, Gullberg, Donald, Noel, Agnès, and Smeland, Hilde Yh
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CANCER invasiveness , *BREAST cancer , *METASTASIS , *CELL migration inhibition , *FIBROBLASTS - Abstract
Cancer-associated fibroblasts (CAFs) are key actors in modulating the progression of many solid tumors such as breast cancer (BC). Herein, we identify an integrin α11/PDGFRβ+ CAF subset displaying tumor-promoting features in BC. In the preclinical MMTV-PyMT mouse model, integrin α11-deficiency led to a drastic reduction of tumor progression and metastasis. A clear association between integrin α11 and PDGFRβ was found at both transcriptional and histological levels in BC specimens. High stromal integrin α11/PDGFRβ expression was associated with high grades and poorer clinical outcome in human BC patients. Functional assays using five CAF subpopulations (one murine, four human) revealed that integrin α11 promotes CAF invasion and CAF-induced tumor cell invasion upon PDGF-BB stimulation. Mechanistically, integrin α11 pro-invasive activity relies on its ability to interact with PDGFRβ in a ligand-dependent manner and to promote its downstream JNK activation, leading to the production of tenascin C, a pro-invasive matricellular protein. Pharmacological inhibition of PDGFRβ and JNK impaired tumor cell invasion induced by integrin α11-positive CAFs. Collectively, our study uncovers an integrin α11-positive subset of pro-tumoral CAFs that exploits PDGFRβ/JNK signalling axis to promote tumor invasiveness in BC. [ABSTRACT FROM AUTHOR]
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- 2019
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15. Radiation-induced myosin IIA expression stimulates collagen type I matrix reorganization.
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Blockhuys, Stéphanie, Van Rompaye, Bart, De Rycke, Riet, Lambein, Kathleen, Claes, Kathleen, Bracke, Marc, De Wagter, Carlos, and De Wever, Olivier
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MYOSIN , *COLLAGEN , *GENE expression , *EXTRACELLULAR matrix , *BREAST cancer , *CANCER radiotherapy , *CANCER cells - Abstract
Abstract: Background and purpose: Extracellular matrix (ECM) reorganization critically contributes to breast cancer (BC) progression and radiotherapy response. We investigated the molecular background and functional consequences of collagen type I (col-I) reorganization by irradiated breast cancer cells (BCC). Materials and methods: Radiation-induced (RI) col-I reorganization was evaluated for MCF-7/6, MCF-7/AZ, T47D and SK-BR-3 BCC. Phase-contrast microscopy and a stressed matrix contraction assay were used for visualization and quantification of col-I reorganization. Cell–matrix interactions were assessed by the inhibition of β1 integrin (neutralizing antibody ‘P5D2’) or focal adhesion kinase (FAK; GSK22560098 small molecule kinase inhibitor). The role of the actomyosin cytoskeleton was explored by western blotting analysis of myosin II expression and activity; and by gene silencing of myosin IIA and pharmacological inhibition of the actomyosin system (blebbistatin, cytochalasin D). BCC death was evaluated by propidium iodide staining. Results: We observed a radiation dose-dependent increase of col-I reorganization by BCC. β1 Integrin/FAK-mediated cell–matrix interactions are essential for RI col-I reorganization. Irradiated BCC are characterized by increased myosin IIA expression and myosin IIA-dependent col-I reorganization. Moreover, RI col-I reorganization by BCC is associated with decreased BCC death, as suggested by pharmacological targeting of the β1 integrin/FAK/myosin IIA pathway. Conclusions: Our data indicate the role of myosin IIA in col-I reorganization by irradiated BCC and reciprocal BCC death. [Copyright &y& Elsevier]
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- 2013
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16. Chitosan/γ-PGA nanoparticles-based immunotherapy as adjuvant to radiotherapy in breast cancer.
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Castro, Flávia, Pinto, Marta L., Pereira, Catarina L., Serre, Karine, Barbosa, Mário A., Vermaelen, Karim, Gärtner, Fátima, Gonçalves, Raquel M., De Wever, Olivier, and Oliveira, Maria J.
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BREAST cancer , *CANCER radiotherapy , *CANCER invasiveness , *TUMOR growth , *TUMOR microenvironment , *GLUTAMIC acid - Abstract
Radiotherapy (RT) is an essential treatment modality for several types of cancer. Despite its therapeutic potential, RT is frequently insufficient to overcome the immunosuppressive nature of the tumor microenvironment, failing to control tumor metastases. Innovative immunomodulatory strategies, like immunostimulatory biomaterials could be used to boost the immunogenic effects of RT. Herein, we addressed the synergistic potential of immunostimulatory chitosan/poly(γ-glutamic acid) nanoparticles (Ch/γ-PGA NPs) combined with RT to induce antitumor immunity in the 4T1 orthotopic breast tumor mouse model. Non-treated animals had progressive primary tumor growth and developed splenomegaly and lung metastases. While RT decreased primary tumor burden, Ch/γ-PGA NPs-treatment decreased systemic immunosuppression and lung metastases. The combination therapy (RT + Ch/γ-PGA NPs) synergistically impaired 4T1 tumor progression, which was associated with a significant primary tumor growth and splenomegaly reduction, a decrease in the percentage of splenic immunosuppressive myeloid cells and an increase in antitumoral CD4+IFN-γ+ population. Notably, animals from the combination therapy presented less and smaller lung metastatic foci and lower levels of the systemic pro-tumor cytokines IL-3, IL-4, IL-10, and of the CCL4 chemokine, in comparison to non-treated animals. Overall, these results evidenced that Ch/γ-PGA NPs potentiate and synergize with RT, headlining their promising role as adjuvant anticancer strategies. Image 1 [ABSTRACT FROM AUTHOR]
- Published
- 2020
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