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Wandernde Tumorzellen identifiziert: Fett beeinflusst Metastasenbildung

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    Wandernde Tumorzellen identifiziert: Fett beeinflusst Metastasenbildung

    Heute auf n-tv erschienen mit Verlinkung zur englischsprachigen Quelle bei "nature": http://www.n-tv.de/wissen/Fett-beein...e19280121.html

    Hier geht's gleich direkt zum Original auf "nature": Targeting metastasis-initiating cells through the fatty acid receptor CD36 (http://www.nature.com/nature/journal...ture20791.html)

    VG Thomas
    Mein Profil bei myProstate.eu

    #2
    Hallo Thomas


    Zitat von spitzmuck Beitrag anzeigen
    Heute auf n-tv erschienen mit Verlinkung zur englischsprachigen Quelle bei "nature": http://www.n-tv.de/wissen/Fett-beein...e19280121.html

    Hier geht's gleich direkt zum Original auf "nature": Targeting metastasis-initiating cells through the fatty acid receptor CD36 (http://www.nature.com/nature/journal...ture20791.html)

    CD36 Antikörper sind immer noch (oder schon wieder) aktuell:

    CD36 mediates palmitate acid-induced metastasis of gastric cancer via AKT/GSK-3β/β-catenin pathway
    "CD36 vermittelt Palmitate Säure-induzierte Metastase von Magenkrebs über AKT / GSK-3β / β-Catenin-Weg" (Übersetzung)
    Background Gastric cancer (GC) has a clear predilection for metastasis toward the omentum which is primarily composed of adipose tissue, indicating that fatty acids may contribute to this phenomenon. However their function remains poorly understood in GC. In this study, we investigated the role of palmitate acid (PA) and its cellular receptor CD36 in the progression of GC. Methods Immunohistochemical (IHC) staining was performed to detect CD36 expression in GC tissues and its clinical significance was determined statistically. CD36 over-expression and knock-down expression cell models were developed and tested in vitro. Wound-healing assays, migration assays, and invasion assays were performed and peritoneal implants into nude mice were done to assess the biological effects of PA and CD36. The underlying mechanisms were investigated using western blot, immunofluorescence (IF), quantitative real-time PCR (qRT-PCR) and antibody blocking assays. Results PA promoted the metastasis of GC by phosphorylation of AKT, which facilitated the nuclear localization of β-catenin through inactivation of GSK-3β via phosphorylation. This tumor-promoting effect of PA was mediated by CD36, a cell surface receptor of fatty acids (FAs). The higher the CD36 expression levels in GC tissues correlated with the poorer the prognosis of patients according to the TCGA database, the GEO database and our own clinical data. Conclusions Our experiments established CD36 as a key mediator of FA-induced metastasis of GC via the AKT/GSK-3β/β-catenin signaling pathway. CD36 might, therefore, constitute a potential therapeutic target for clinical intervention in GC.



    siehe auch
    Was Metastasen so gefährlich macht


    Rudi

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