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  1. Article ; Online: Correction: The angiogenesis suppressor gene AKAP12 is under the epigenetic control of HDAC7 in endothelial cells.

    Turtoi, Andrei / Mottet, Denis / Matheus, Nicolas / Dumont, Bruno / Peixoto, Paul / Hennequière, Vincent / Deroanne, Christophe / Colige, Alain / De Pauw, Edwin / Bellahcène, Akeila / Castronovo, Vincent

    Angiogenesis

    2023  Volume 27, Issue 1, Page(s) 121–122

    Language English
    Publishing date 2023-11-07
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 1484717-6
    ISSN 1573-7209 ; 0969-6970
    ISSN (online) 1573-7209
    ISSN 0969-6970
    DOI 10.1007/s10456-023-09898-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5094: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Myoferlin controls mitochondrial structure and activity in pancreatic ductal adenocarcinoma, and affects tumor aggressiveness.

    Rademaker, Gilles / Hennequière, Vincent / Brohée, Laura / Nokin, Marie-Julie / Lovinfosse, Pierre / Durieux, Florence / Gofflot, Stéphanie / Bellier, Justine / Costanza, Brunella / Herfs, Michael / Peiffer, Raphael / Bettendorff, Lucien / Deroanne, Christophe / Thiry, Marc / Delvenne, Philippe / Hustinx, Roland / Bellahcène, Akeila / Castronovo, Vincent / Peulen, Olivier

    Oncogene

    2018  Volume 37, Issue 32, Page(s) 4398–4412

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Therapeutic options remain very limited and are based on classical chemotherapies. Energy metabolism reprogramming appears as an emerging hallmark of cancer and ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related death. Therapeutic options remain very limited and are based on classical chemotherapies. Energy metabolism reprogramming appears as an emerging hallmark of cancer and is considered a therapeutic target with considerable potential. Myoferlin, a ferlin family member protein overexpressed in PDAC, is involved in plasma membrane biology and has a tumor-promoting function. In the continuity of our previous studies, we investigated the role of myoferlin in the context of energy metabolism in PDAC. We used selected PDAC tumor samples and PDAC cell lines together with small interfering RNA technology to study the role of myoferlin in energetic metabolism. In PDAC patients, we showed that myoferlin expression is negatively correlated with overall survival and with glycolytic activity evaluated by
    MeSH term(s) Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Adenosine Triphosphate/metabolism ; Autophagy/physiology ; Calcium-Binding Proteins/metabolism ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Proliferation/physiology ; Energy Metabolism/physiology ; Gene Expression Regulation, Neoplastic/physiology ; Glycolysis/physiology ; Humans ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondria/pathology ; Muscle Proteins/metabolism ; Oxidative Phosphorylation ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; RNA, Small Interfering/metabolism
    Chemical Substances Calcium-Binding Proteins ; MYOF protein, human ; Membrane Proteins ; Muscle Proteins ; RNA, Small Interfering ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2018-05-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-018-0287-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2218: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  3. Article ; Online: Innovative methodology for the identification of soluble biomarkers in fresh tissues.

    Costanza, Brunella / Turtoi, Andrei / Bellahcène, Akeila / Hirano, Touko / Peulen, Olivier / Blomme, Arnaud / Hennequière, Vincent / Mutijima, Eugene / Boniver, Jacques / Meuwis, Marie-Alice / Josse, Claire / Koopmansch, Benjamin / Segers, Karin / Yokobori, Takehiko / Fahmy, Karim / Thiry, Marc / Coimbra, Carla / Garbacki, Nancy / Colige, Alain /
    Baiwir, Dominique / Bours, Vincent / Louis, Edouard / Detry, Olivier / Delvenne, Philippe / Nishiyama, Masahiko / Castronovo, Vincent

    Oncotarget

    2018  Volume 9, Issue 12, Page(s) 10665–10680

    Abstract: The identification of diagnostic and prognostic biomarkers from early lesions, measurable in liquid biopsies remains a major challenge, particularly in oncology. Fresh human material of high quality is required for biomarker discovery but is often not ... ...

    Abstract The identification of diagnostic and prognostic biomarkers from early lesions, measurable in liquid biopsies remains a major challenge, particularly in oncology. Fresh human material of high quality is required for biomarker discovery but is often not available when it is totally required for clinical pathology investigation. Hence, all OMICs studies are done on residual and less clinically relevant biological samples. Here after, we present an innovative, simple, and non-destructive, procedure named EXPEL that uses rapid, pressure-assisted, interstitial fluid extrusion, preserving the specimen for full routine clinical pathology investigation. In the meantime, the technique allows a comprehensive OMICs analysis (proteins, metabolites, miRNAs and DNA). As proof of concept, we have applied EXPEL on freshly collected human colorectal cancer and liver metastases tissues. We demonstrate that the procedure efficiently allows the extraction, within a few minutes, of a wide variety of biomolecules holding diagnostic and prognostic potential while keeping both tissue morphology and antigenicity unaltered. Our method enables, for the first time, both clinicians and scientists to explore identical clinical material regardless of its origin and size, which has a major positive impact on translation to the clinic.
    Language English
    Publishing date 2018-02-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.24366
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Myoferlin is a key regulator of EGFR activity in breast cancer.

    Turtoi, Andrei / Blomme, Arnaud / Bellahcène, Akeila / Gilles, Christine / Hennequière, Vincent / Peixoto, Paul / Bianchi, Elettra / Noel, Agnès / De Pauw, Edwin / Lifrange, Eric / Delvenne, Philippe / Castronovo, Vincent

    Cancer research

    2013  Volume 73, Issue 17, Page(s) 5438–5448

    Abstract: Myoferlin is a member of the ferlin family of proteins that participate in plasma membrane fusion, repair, and endocytosis. While some reports have implicated myoferlin in cancer, the extent of its expression in and contributions to cancer are not well ... ...

    Abstract Myoferlin is a member of the ferlin family of proteins that participate in plasma membrane fusion, repair, and endocytosis. While some reports have implicated myoferlin in cancer, the extent of its expression in and contributions to cancer are not well established. In this study, we show that myoferlin is overexpressed in human breast cancers and that it has a critical role in controlling degradation of the epidermal growth factor (EGF) receptor (EGFR) after its activation and internalization in breast cancer cells. Myoferlin depletion blocked EGF-induced cell migration and epithelial-to-mesenchymal transition. Both effects were induced as a result of impaired degradation of phosphorylated EGFR via dysfunctional plasma membrane caveolae and alteration of caveolin homo-oligomerization. In parallel, myoferlin depletion reduced tumor development in a chicken chorioallantoic membrane xenograft model of human breast cancer. Considering the therapeutic significance of EGFR targeting, our findings identify myoferlin as a novel candidate function to target for future drug development.
    MeSH term(s) Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Animals ; Apoptosis ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Calcium-Binding Proteins/antagonists & inhibitors ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Carcinoma, Ductal, Breast/metabolism ; Carcinoma, Ductal, Breast/pathology ; Carcinoma, Lobular/metabolism ; Carcinoma, Lobular/pathology ; Caveolae/metabolism ; Cell Movement ; Cell Proliferation ; Chick Embryo ; Chorioallantoic Membrane/metabolism ; Epidermal Growth Factor/pharmacology ; Epithelial-Mesenchymal Transition ; Female ; Fluorescent Antibody Technique ; Gene Expression Regulation, Neoplastic ; Glycolysis ; Humans ; Immunoenzyme Techniques ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Muscle Proteins/antagonists & inhibitors ; Muscle Proteins/genetics ; Muscle Proteins/metabolism ; Neoplasm Invasiveness ; Proteomics ; RNA, Small Interfering/genetics ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/genetics ; Receptor, Epidermal Growth Factor/metabolism ; Tumor Cells, Cultured
    Chemical Substances Calcium-Binding Proteins ; MYOF protein, human ; Membrane Proteins ; Muscle Proteins ; RNA, Small Interfering ; Epidermal Growth Factor (62229-50-9) ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2013-09-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-13-1142
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: The angiogenesis suppressor gene AKAP12 is under the epigenetic control of HDAC7 in endothelial cells.

    Turtoi, Andrei / Mottet, Denis / Matheus, Nicolas / Dumont, Bruno / Peixoto, Paul / Hennequière, Vincent / Deroanne, Christophe / Colige, Alain / De Pauw, Edwin / Bellahcène, Akeila / Castronovo, Vincent

    Angiogenesis

    2012  Volume 15, Issue 4, Page(s) 543–554

    Abstract: Histone deacetylases (HDACs) are a family of 18 enzymes that deacetylate lysine residues of both histone and nonhistone proteins and to a large extent govern the process of angiogenesis. Previous studies have shown that specific inhibition of HDAC7 ... ...

    Abstract Histone deacetylases (HDACs) are a family of 18 enzymes that deacetylate lysine residues of both histone and nonhistone proteins and to a large extent govern the process of angiogenesis. Previous studies have shown that specific inhibition of HDAC7 blocks angiogenesis both in vitro and in vivo. However, the underlying molecular mechanisms are not fully understood and hence preclude any meaningful development of suitable therapeutic modalities. The goal of the present study was to further the understanding of HDAC7 epigenetic control of angiogenesis in human endothelial cells using the proteomic approach. The underlying problem was approached through siRNA-mediated gene-expression silencing of HDAC7 in human umbilical vein endothelial cells (HUVECs). To this end, HUVEC proteins were extracted and proteomically analyzed. The emphasis was placed on up-regulated proteins, as these may represent potential direct epigenetic targets of HDAC7. Among several proteins, A-kinase anchor protein 12 (AKAP12) was the most reproducibly up-regulated protein following HDAC7 depletion. This overexpression of AKAP12 was responsible for the inhibition of migration and tube formation in HDAC7-depleted HUVEC. Mechanistically, H3 histones associated with AKAP12 promoter were acetylated following the removal of HDAC7, leading to an increase in its mRNA and protein levels. AKAP12 is responsible for protein kinase C mediated phosphorylation of signal transducer and activator of transcription 3 (STAT3). Phosphorylated STAT3 increasingly binds to the chromatin and AKAP12 promoter and is necessary for maintaining the elevated levels of AKAP12 following HDAC7 knockdown. We demonstrated for the first time that AKAP12 tumor/angiogenesis suppressor gene is an epigenetic target of HDAC7, whose elevated levels lead to a negative regulation of HUVEC migration and inhibit formation of tube-like structures.
    MeSH term(s) A Kinase Anchor Proteins/genetics ; Base Sequence ; Cell Cycle Proteins/genetics ; Cells, Cultured ; Chromatin Immunoprecipitation ; Endothelium, Vascular/cytology ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/metabolism ; Epigenesis, Genetic ; Histone Deacetylases/metabolism ; Humans ; Intercellular Adhesion Molecule-1/physiology ; Neovascularization, Physiologic/genetics ; Phosphorylation ; Promoter Regions, Genetic ; Protein Kinase C/metabolism ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism
    Chemical Substances A Kinase Anchor Proteins ; AKAP12 protein, human ; Cell Cycle Proteins ; RNA, Small Interfering ; STAT3 Transcription Factor ; STAT3 protein, human ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Protein Kinase C (EC 2.7.11.13) ; HDAC7 protein, human (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2012-05-15
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1484717-6
    ISSN 1573-7209 ; 0969-6970
    ISSN (online) 1573-7209
    ISSN 0969-6970
    DOI 10.1007/s10456-012-9279-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5094: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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