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  1. Article: Activation of bile salt dependent lipase by (lyso)phosphatidic acid and platelet activating factor

    Fontbonne, Hervé / Antoine Puigserver / Bernard Bouza / Dominique Lombardo / El Hassan Ajandouz

    Federation of European Biochemical Societies FEBS letters. 2013 Sept. 17, v. 587, no. 18

    2013  

    Abstract: The activity of breast milk BSDL was assayed with or without phospholipids as extra-intestinal effector candidates. Phosphatidic acid, lysophosphatidic acid and platelet activating factor but not phosphatidylcholine and lysophosphatidylcholine stimulated ...

    Abstract The activity of breast milk BSDL was assayed with or without phospholipids as extra-intestinal effector candidates. Phosphatidic acid, lysophosphatidic acid and platelet activating factor but not phosphatidylcholine and lysophosphatidylcholine stimulated BSDL activity at least as efficiently as taurocholate. The apparent dissociation constants of PA and LPA at saturating concentrations of three different substrates were between 0.1 and 13.4μM and that of PAF was below or equal to 200pM. Kinetic data suggested the existence of at least one binding site for each of these effectors. PA, LPA and PAF are likely extra-intestinal modulators of BSDL activity.
    Keywords bile salts ; binding sites ; breast milk ; dissociation ; lysophosphatidylcholine ; platelet-activating factor
    Language English
    Dates of publication 2013-0917
    Size p. 3002-3007.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2013.07.020
    Database NAL-Catalogue (AGRICOLA)

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  2. Article ; Online: Saccharomyces boulardii improves intestinal epithelial cell restitution by inhibiting αvβ5 integrin activation state.

    Alexandra Canonici / Emilie Pellegrino / Carole Siret / Chloé Terciolo / Dorota Czerucka / Sonia Bastonero / Jacques Marvaldi / Dominique Lombardo / Véronique Rigot / Frédéric André

    PLoS ONE, Vol 7, Iss 9, p e

    2012  Volume 45047

    Abstract: Intestinal epithelial cell damage is frequently seen in the mucosal lesions of infectious or inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. Complete remission of these diseases requires both the disappearance of inflammation ... ...

    Abstract Intestinal epithelial cell damage is frequently seen in the mucosal lesions of infectious or inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. Complete remission of these diseases requires both the disappearance of inflammation and the repair of damaged epithelium. Saccharomyces boulardii (Sb, Biocodex) is a non-pathogenic yeast widely used as a preventive and therapeutic probiotic for the prevention and treatment of diarrhea and other gastrointestinal disorders. We recently showed that it enhances the repair of intestinal epithelium through activation of α2β1 integrin collagen receptors. In the present study, we demonstrated that α2β1 integrin is not the sole cell-extracellular matrix receptor involved during Sb-mediated intestinal restitution. Indeed, by using cell adhesion assays, we showed that Sb supernatant contains heat sensitive molecule(s), with a molecular weight higher than 9 kDa, which decreased αvβ5 integrin-mediated adhesion to vitronectin by competing with the integrin. Moreover, Sb-mediated changes in cell adhesion to vitronectin resulted in a reduction of the αvβ5signaling pathway. We used a monolayer wounding assay that mimics in vivo cell restitution to demonstrate that down-modulation of the αvβ5 integrin-vitronectin interaction is related to Sb-induced cell migration. We therefore postulated that Sb supernatant contains motogenic factors that enhance cell restitution through multiple pathways, including the dynamic fine regulation of αvβ5 integrin binding activity. This could be of major importance in diseases characterized by severe mucosal injury, such as inflammatory and infectious bowel diseases.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Exosomal lipids impact notch signaling and induce death of human pancreatic tumoral SOJ-6 cells.

    Sadia Beloribi / Elodie Ristorcelli / Gilles Breuzard / Françoise Silvy / Justine Bertrand-Michel / Evelyne Beraud / Alain Verine / Dominique Lombardo

    PLoS ONE, Vol 7, Iss 10, p e

    2012  Volume 47480

    Abstract: Exosomes are of increasing interest as alternative mode of cell-to-cell communication. We previously reported that exosomes secreted by human SOJ-6 pancreatic tumor cells induce (glyco)protein ligand-independent cell death and inhibit Notch-1 pathway, ... ...

    Abstract Exosomes are of increasing interest as alternative mode of cell-to-cell communication. We previously reported that exosomes secreted by human SOJ-6 pancreatic tumor cells induce (glyco)protein ligand-independent cell death and inhibit Notch-1 pathway, this latter being particularly active during carcinogenesis and in cancer stem cells. Therefore, we asked whether exosomal lipids were key-elements for cell death and hypothesized that cholesterol-rich membrane microdomains were privileged sites of exosome interactions with tumor cells. To address these questions and based on the lipid composition of exosomes from SOJ-6 cells (Ristorcelli et al. (2008) FASEB J. 22; 3358-3369) enriched in cholesterol and sphingomyelin (lipids forming liquid-ordered phase, Lo) and depleted in phospholipids (lipids forming liquid-disordered phase, Ld), we designed Synthetic Exosome-Like Nanoparticles (SELN) with ratios Lo/Ld from 3.0 to 6.0 framing that of SOJ-6 cell exosomes. SELN decreased tumor cell survival, the higher the Lo/Ld ratio, the lower the cell survival. This decreased survival was due to activation of cell death with inhibition of Notch pathway. FRET analyses indicated fusions/exchanges of SELN with cell membranes. Fluorescent SELN co-localized with the ganglioside GM1 then with Rab5A, markers of lipid microdomains and of early endosomes, respectively. These interactions occurred at lipid microdomains of plasma and/or endosome membranes where the Notch-1 pathway matures. We thus demonstrated a major role for lipids in interactions between SELN and tumor cells, and in the ensued cell death. To our knowledge this is the first report on such effects of lipidic nanoparticles on tumor cell behavior. This may have implications in tumor progression.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Collagen-derived proline promotes pancreatic ductal adenocarcinoma cell survival under nutrient limited conditions

    Orianne Olivares / Jared R. Mayers / Victoire Gouirand / Margaret E. Torrence / Tristan Gicquel / Laurence Borge / Sophie Lac / Julie Roques / Marie-Noëlle Lavaut / Patrice Berthezène / Marion Rubis / Veronique Secq / Stéphane Garcia / Vincent Moutardier / Dominique Lombardo / Juan Lucio Iovanna / Richard Tomasini / Fabienne Guillaumond / Matthew G. Vander Heiden /
    Sophie Vasseur

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Volume 14

    Abstract: Cancer cells adapt their metabolism to survive limited nutrient availability. Here, the authors show that in conditions of limited glucose or glutamine availability, pancreatic ductal adenocarcinoma cells can use collagen-derived proline to foster the ... ...

    Abstract Cancer cells adapt their metabolism to survive limited nutrient availability. Here, the authors show that in conditions of limited glucose or glutamine availability, pancreatic ductal adenocarcinoma cells can use collagen-derived proline to foster the TCA cycle and allow cell survival bothin vitro and in vivo.
    Keywords Science ; Q
    Language English
    Publishing date 2017-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Further characterization of HDAC and SIRT gene expression patterns in pancreatic cancer and their relation to disease outcome.

    Mehdi Ouaïssi / Françoise Silvy / Céline Loncle / Diva Ferraz da Silva / Carla Martins Abreu / Emmanuelle Martinez / Patrick Berthézene / Sophie Cadra / Yves Patrice Le Treut / Jean Hardwigsen / Bernard Sastre / Igor Sielezneff / Liliane Benkoel / Jean Delgrande / Ali Ouaissi / Juan Iovanna / Dominique Lombardo / Eric Mas

    PLoS ONE, Vol 9, Iss 9, p e

    2014  Volume 108520

    Abstract: Ductal adenocarcinoma of the pancreas is ranking 4 for patient' death from malignant disease in Western countries, with no satisfactory treatment. We re-examined more precisely the histone deacetylases (HDAC) and Sirtuin (SIRT) gene expression patterns ... ...

    Abstract Ductal adenocarcinoma of the pancreas is ranking 4 for patient' death from malignant disease in Western countries, with no satisfactory treatment. We re-examined more precisely the histone deacetylases (HDAC) and Sirtuin (SIRT) gene expression patterns in pancreatic cancer with more pancreatic tumors and normal tissues. We also examined the possible relationship between HDAC gene expression levels and long term disease outcome. Moreover, we have evaluated by using an in vitro model system of human pancreatic tumor cell line whether HDAC7 knockdown may affect the cell behavior. We analyzed 29 pancreatic adenocarcinoma (PA), 9 chronic pancreatitis (CP), 8 benign pancreatic (BP) and 11 normal pancreatic tissues. Concerning pancreatic adenocarcinoma, we were able to collect biopsies at the tumor periphery. To assess the possible involvement of HDAC7 in cell proliferation capacity, we have generated recombinant human Panc-1 tumor which underexpressed or overexpressed HDAC7. The expression of HDAC1,2,3,4,7 and Nur77 increased in PA samples at levels significantly higher than those observed in the CP group (p = 0.0160; 0.0114; 0.0227; 0.0440; 0.0136; 0.0004, respectively). The expression of HDAC7, was significantly greater in the PA compared with BP tissue samples (p = 0.05). Mean mRNA transcription levels of PA for HDAC7 and HDAC2 were higher when compared to their counterpart biopsies taken at the tumor periphery (p = 0.0346, 0.0053, respectively). Moreover, the data obtained using confocal microscopy and a quantitative method of immunofluorescence staining strongly support the HDAC7 overexpression in PA surgical specimens. The number of deaths and recurrences at the end of follow up were significantly greater in patients with overexpression of HDAC7. Interestingly, the rate of growth was significantly reduced in the case of cell carrying shRNA construct targeting HDAC7 encoding gene when compared to the parental Panc-1 tumor cells (p = 0.0015) at 48 h and 96 h (p = 0.0021). This study strongly support the notion ...
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: HDAC gene expression in pancreatic tumor cell lines following treatment with the HDAC inhibitors panobinostat (LBH589) and trichostatine (TSA).

    Mehdi, Ouaïssi / Françoise, Silvy / Sofia, Costa Lima / Urs, Giger / Kevin, Zemmour / Bernard, Sastre / Igor, Sielezneff / Anabela, Cordeiro-da-Silva / Dominique, Lombardo / Eric, Mas / Ali, Ouaïssi

    Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

    2012  Volume 12, Issue 2, Page(s) 146–155

    Abstract: Background: In this study, the effect of LBH589 and trichostatin (TSA), a standard histone deacetylase inhibitor (HDACi) toward the growth of pancreatic cancer cell lines was studied. Thus, we examined for the first time, the HDAC family gene expression ...

    Abstract Background: In this study, the effect of LBH589 and trichostatin (TSA), a standard histone deacetylase inhibitor (HDACi) toward the growth of pancreatic cancer cell lines was studied. Thus, we examined for the first time, the HDAC family gene expression levels before and after drug treatment.
    Methods: Several human pancreatic cancer cell lines (Panc-1, BxPC-3, SOJ-6) and a normal human pancreatic duct immortalized epithelial cell line (HPDE/E6E7) were used as target cells. The cell growth was measured by MTT assay, cell cycle alteration, membrane phosphatidylserine exposure, DNA fragmentation, mitochondrial membrane potential loss, RT-PCR and Western blots were done using standard methods. The effect of drugs on tumor growth in vivo was studied using subcutaneous xenograft model.
    Results: Except in the case of certain HDAC gene/tumor cell line couples: (SIRT1/HPDE-SOJ6/TSA- or LBH589-treated cells; LBH589-treated Panc-1 Cells; HDAC2/BxPC-3/LBH589-treated cells or TSA-treated SOJ-6-1 cells), there were no major significant changes of HDACs genes transcription in cells upon drug treatment. However, significant variation in HDACs and SIRTs protein expression levels could be seen among individual cell samples. The in vivo results showed that LBH589 formulation exhibited similar tumor reduction efficacy as the commercial drug gemcitabine.
    Conclusion: Our data demonstrate that LBH589 induced the death of pancreatic tumor cell by apoptosis. In line with its in vitro activity, LBH589 achieved a significant reduction in tumor growth in BxPC-3 pancreatic tumor cell line subcutaneous xenograft mouse model. Furthermore, exploring the impact of LBH589 on HDACs encoding genes expression revealed for the first time that some of them, depending on the cell line considered, seem to be regulated during translation.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Drug Screening Assays, Antitumor ; Epithelial Cells/drug effects ; Epithelial Cells/pathology ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Indoles/pharmacology ; Membrane Potential, Mitochondrial/drug effects ; Mice ; Mice, Nude ; Pancreatic Ducts/drug effects ; Pancreatic Ducts/pathology ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; RNA, Messenger/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Treatment Outcome
    Chemical Substances Antineoplastic Agents ; Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Indoles ; RNA, Messenger ; trichostatin A (3X2S926L3Z) ; panobinostat (9647FM7Y3Z) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2012-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2056680-3
    ISSN 1424-3911 ; 1424-3903
    ISSN (online) 1424-3911
    ISSN 1424-3903
    DOI 10.1016/j.pan.2012.02.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Monoclonal Antibody 16D10 to the C-Terminal Domain of the Feto-Acinar Pancreatic Protein Binds to Membrane of Human Pancreatic Tumoral SOJ-6 Cells and Inhibits the Growth of Tumor Xenografts

    Laurence Panicot-Dubois / Muriel Aubert / Cécile Franceschi / Eric Mas / Françoise Silvy / Christian Crotte / Jean-Paul Bernard / Dominique Lombardo / Marie-Odile Sadoulet

    Neoplasia : An International Journal for Oncology Research, Vol 6, Iss 6, Pp 713-

    2004  Volume 724

    Abstract: Feto-acinar pancreatic protein (FAPP) characterized by mAbJ28 reactivity is a specific component associated with ontogenesis and behaves as an oncodevelopment-associated antigen. We attempted to determine whether pancreatic tumoral SOJ-6 cells are ... ...

    Abstract Feto-acinar pancreatic protein (FAPP) characterized by mAbJ28 reactivity is a specific component associated with ontogenesis and behaves as an oncodevelopment-associated antigen. We attempted to determine whether pancreatic tumoral SOJ-6 cells are expressed at their surface FAPP antigens and to examine if specific antibodies directed against these FAPP epitopes could decrease the growth of pancreatic tumors in a mice model. For this purpose, we used specific antibodies against either the whole FAPP, the O-glycosylated C-terminal domain, or the N-terminal domain of the protein. Our results indicate that SOJ-6 cells expressed at their surface a 32-kDa peptide corresponding to the C-terminal domain of the FAPP. Furthermore, we show, by using endoproteinase Lys-C or geldanamycin, a drug able to impair the FAPP secretion, that this 32-kDa peptide expressed on the SOJ-6 cell surface comes from the degradation of the FAPP. Finally, an in vivo prospective study using a preventative tumor model in nude mice indicates that targeting this peptide by the use of mAb16D10 inhibits the growth of SOJ-6 xenografts. The specificity of mAb16D10 for pancreatic tumors and the possibility to obtain recombinant structures of mucin-like peptides recognized by mAb16D10 and mAbJ28 are promising tools in immunologic approaches to cure pancreatic cancers.
    Keywords Pancreas ; cancer ; bile salt-dependent lipase (BSDL) ; feto-acinar pancreatic protein (FAPP) ; monoclonal antibody ; Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Subject code 572
    Publishing date 2004-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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