Tumor-derived fibulin-3 activates pro-invasive NF-κB signaling in glioblastoma cells and their microenvironment.
作者： M S Nandhu , A Kwiatkowska , V Bhaskaran , J Hayes , B Hu
DOI: 10.1038/ONC.2017.109
关键词: Signal transduction 、 Cell biology 、 Tumor progression 、 Fibulin 、 Biology 、 Growth factor receptor 、 Glioma 、 Tumor Virus 、 Tumor microenvironment 、 Tumor-Derived
摘要: Molecular profiling of glioblastomas has revealed the presence key signaling hubs that contribute to tumor progression and acquisition resistance. One these main mechanisms is nuclear factor-kappa B (NF-κB) pathway, which integrates multiple extracellular signals into transcriptional programs for growth, invasion maintenance tumor-initiating population. We show here an protein released by glioblastoma cells, fibulin-3, drives oncogenic NF-κB in increases activation peritumoral astrocytes. Fibulin-3 expression correlates with a NF-κB-regulated 'invasive signature' linked poorer survival, being possible tissue marker regions active progression. Accordingly, fibulin-3 promotes manner requires both cells their microenvironment. Mechanistically, we found activates metalloprotease ADAM17 competing its endogenous inhibitor, TIMP3. This results sustained release soluble necrosis factor alpha (TNFα) ADAM17, turn TNF receptors canonical signaling. Taken together, our underscore as novel signal strong activating effect on malignant gliomas. Because produced de novo tumors absent from normal brain, propose targeting fibulin-3/NF-κB axis may provide avenue disrupt combination therapies brain tumors.
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