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  1. Article ; Online: The 5-lipoxygenase/cyclooxygenase-2 cross-over metabolite, hemiketal E

    Nakashima, Fumie / Giménez-Bastida, Juan A / Luis, Paula B / Presley, Sai H / Boer, Robert E / Chiusa, Manuel / Shibata, Takahiro / Sulikowski, Gary A / Pozzi, Ambra / Schneider, Claus

    The Journal of biological chemistry

    2023  Volume 299, Issue 4, Page(s) 103050

    Abstract: Consecutive oxygenation of arachidonic acid by 5-lipoxygenase and cyclooxygenase-2 yields the hemiketal eicosanoids, ... ...

    Abstract Consecutive oxygenation of arachidonic acid by 5-lipoxygenase and cyclooxygenase-2 yields the hemiketal eicosanoids, HKE
    MeSH term(s) Mice ; Humans ; Animals ; Cyclooxygenase 2/metabolism ; Arachidonic Acid ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Arachidonate 5-Lipoxygenase ; Vascular Endothelial Growth Factor A/metabolism ; Neovascularization, Physiologic ; Human Umbilical Vein Endothelial Cells/metabolism ; Angiogenesis Inhibitors/pharmacology ; Cell Movement ; Cell Proliferation
    Chemical Substances Cyclooxygenase 2 (EC 1.14.99.1) ; Arachidonic Acid (27YG812J1I) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Arachidonate 5-Lipoxygenase (EC 1.13.11.34) ; Vascular Endothelial Growth Factor A ; Angiogenesis Inhibitors
    Language English
    Publishing date 2023-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.103050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma.

    Williams, Christopher S / Zhang, Baolin / Smith, J Joshua / Jayagopal, Ashwath / Barrett, Caitlyn W / Pino, Christopher / Russ, Patricia / Presley, Sai H / Peng, DunFa / Rosenblatt, Daniel O / Haselton, Frederick R / Yang, Jin-Long / Washington, M Kay / Chen, Xi / Eschrich, Steven / Yeatman, Timothy J / El-Rifai, Wael / Beauchamp, R Daniel / Chang, Min S

    The Journal of clinical investigation

    2011  Volume 121, Issue 10, Page(s) 4056–4069

    Abstract: The acquisition of a mesenchymal phenotype is a critical step in the metastatic progression of epithelial carcinomas. Adherens junctions (AJs) are required for suppressing this epithelial-mesenchymal transition (EMT) but less is known about the role of ... ...

    Abstract The acquisition of a mesenchymal phenotype is a critical step in the metastatic progression of epithelial carcinomas. Adherens junctions (AJs) are required for suppressing this epithelial-mesenchymal transition (EMT) but less is known about the role of tight junctions (TJs) in this process. Here, we investigated the functions of blood vessel epicardial substance (BVES, also known as POPDC1 and POP1), an integral membrane protein that regulates TJ formation. BVES was found to be underexpressed in all stages of human colorectal carcinoma (CRC) and in adenomatous polyps, indicating its suppression occurs early in transformation. Similarly, the majority of CRC cell lines tested exhibited decreased BVES expression and promoter DNA hypermethylation, a modification associated with transcriptional silencing. Treatment with a DNA-demethylating agent restored BVES expression in CRC cell lines, indicating that methylation represses BVES expression. Reexpression of BVES in CRC cell lines promoted an epithelial phenotype, featuring decreased proliferation, migration, invasion, and anchorage-independent growth; impaired growth of an orthotopic xenograft; and blocked metastasis. Conversely, interfering with BVES function by expressing a dominant-negative mutant in human corneal epithelial cells induced mesenchymal features. These biological outcomes were associated with changes in AJ and TJ composition and related signaling. Therefore, BVES prevents EMT, and its epigenetic silencing may be an important step in promoting EMT programs during colon carcinogenesis.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Adenocarcinoma/physiopathology ; Adherens Junctions/pathology ; Adherens Junctions/physiology ; Animals ; Cell Adhesion Molecules ; Cell Line, Tumor ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Colonic Neoplasms/physiopathology ; Colonic Polyps/genetics ; Colonic Polyps/pathology ; Colonic Polyps/physiopathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/physiopathology ; DNA Methylation ; Epithelial-Mesenchymal Transition/genetics ; Epithelial-Mesenchymal Transition/physiology ; Epithelium, Corneal/cytology ; Epithelium, Corneal/physiology ; Gene Expression ; Gene Silencing ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/physiology ; Mice ; Mice, Nude ; Muscle Proteins ; Mutation ; Neoplasm Transplantation ; Promoter Regions, Genetic ; Signal Transduction ; Tight Junctions/pathology ; Tight Junctions/physiology ; Transplantation, Heterologous
    Chemical Substances BVES protein, human ; Cell Adhesion Molecules ; Membrane Proteins ; Muscle Proteins
    Language English
    Publishing date 2011-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI44228
    Database MEDical Literature Analysis and Retrieval System OnLINE

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