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  1. AU="Shruti A. Anant"
  2. AU="Jin, Hong-Wei"
  3. AU="Gonzalez, Louis"
  4. AU=Torres Victor J.
  5. AU="Manning, Nyla"
  6. AU="Sindkar, Anushka"
  7. AU=Rodieux Frdrique
  8. AU="Tote, Sachin"

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  1. Artikel ; Online: SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactions

    Jennifer M. Pilat / Rachel E. Brown / Zhengyi Chen / Nathaniel J. Berle / Adrian P. Othon / M. Kay Washington / Shruti A. Anant / Suguru Kurokawa / Victoria H. Ng / Joshua J. Thompson / Justin Jacobse / Jeremy A. Goettel / Ethan Lee / Yash A. Choksi / Ken S. Lau / Sarah P. Short / Christopher S. Williams

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 13

    Abstract: Although selenium deficiency correlates with colorectal cancer (CRC) risk, the roles of the selenium-rich antioxidant selenoprotein P (SELENOP) in CRC remain unclear. In this study, we defined SELENOP’s contributions to sporadic CRC. In human single-cell ...

    Abstract Although selenium deficiency correlates with colorectal cancer (CRC) risk, the roles of the selenium-rich antioxidant selenoprotein P (SELENOP) in CRC remain unclear. In this study, we defined SELENOP’s contributions to sporadic CRC. In human single-cell cRNA-Seq (scRNA-Seq) data sets, we discovered that SELENOP expression rose as normal colon stem cells transformed into adenomas that progressed into carcinomas. We next examined the effects of Selenop KO in a mouse adenoma model that involved conditional, intestinal epithelium-specific deletion of the tumor suppressor adenomatous polyposis coli (Apc) and found that Selenop KO decreased colon tumor incidence and size. We mechanistically interrogated SELENOP-driven phenotypes in tumor organoids as well as in CRC and noncancer cell lines. Selenop-KO tumor organoids demonstrated defects in organoid formation and decreases in WNT target gene expression, which could be reversed by SELENOP restoration. Moreover, SELENOP increased canonical WNT signaling activity in noncancer and CRC cell lines. In defining the mechanism of action of SELENOP, we mapped protein-protein interactions between SELENOP and the WNT coreceptors low-density lipoprotein receptor–related proteins 5 and 6 (LRP5/6). Last, we confirmed that SELENOP-LRP5/6 interactions contributed to the effects of SELENOP on WNT activity. Overall, our results position SELENOP as a modulator of the WNT signaling pathway in sporadic CRC.
    Schlagwörter Gastroenterology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-07-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors

    Rachel E. Brown / Justin Jacobse / Shruti A. Anant / Koral M. Blunt / Bob Chen / Paige N. Vega / Chase T. Jones / Jennifer M. Pilat / Frank Revetta / Aidan H. Gorby / Kristy R. Stengel / Yash A. Choksi / Kimmo Palin / M. Blanca Piazuelo / Mary Kay Washington / Ken S. Lau / Jeremy A. Goettel / Scott W. Hiebert / Sarah P. Short /
    Christopher S. Williams

    JCI Insight, Vol 7, Iss

    2022  Band 10

    Abstract: Aberrant epithelial differentiation and regeneration contribute to colon pathologies, including inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Myeloid translocation gene 16 (MTG16, also known as CBFA2T3) is a transcriptional ... ...

    Abstract Aberrant epithelial differentiation and regeneration contribute to colon pathologies, including inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Myeloid translocation gene 16 (MTG16, also known as CBFA2T3) is a transcriptional corepressor expressed in the colonic epithelium. MTG16 deficiency in mice exacerbates colitis and increases tumor burden in CAC, though the underlying mechanisms remain unclear. Here, we identified MTG16 as a central mediator of epithelial differentiation, promoting goblet and restraining enteroendocrine cell development in homeostasis and enabling regeneration following dextran sulfate sodium–induced (DSS-induced) colitis. Transcriptomic analyses implicated increased Ephrussi box–binding transcription factor (E protein) activity in MTG16-deficient colon crypts. Using a mouse model with a point mutation that attenuates MTG16:E protein interactions (Mtg16P209T), we showed that MTG16 exerts control over colonic epithelial differentiation and regeneration by repressing E protein–mediated transcription. Mimicking murine colitis, MTG16 expression was increased in biopsies from patients with active IBD compared with unaffected controls. Finally, uncoupling MTG16:E protein interactions partially phenocopied the enhanced tumorigenicity of Mtg16–/– colon in the azoxymethane/DSS-induced model of CAC, indicating that MTG16 protects from tumorigenesis through additional mechanisms. Collectively, our results demonstrate that MTG16, via its repression of E protein targets, is a key regulator of cell fate decisions during colon homeostasis, colitis, and cancer.
    Schlagwörter Cell biology ; Gastroenterology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-05-01T00:00:00Z
    Verlag American Society for Clinical investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

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