Suppression of G-protein-coupled receptor kinase 3 expression is a feature of classical GBM that is required for maximal growth.

ABSTRACT: G-protein-coupled receptor kinases (GRK) regulate the function of G-protein-coupled receptors (GPCR). Previously, we found that GPCR (CXCR4)-mediated astrocytoma growth was dependent upon abnormally sustained CXCR4 signaling and was correlated with decreased GRK-mediated receptor phosphorylation. As CXCR4 has also been implicated in the stimulation of high-grade glioma growth, we sought to determine whether dysregulation of GRK expression and/or function might also be present in high-grade gliomas. In an analysis of data from The Cancer Genome Atlas, we found that GRK3 expression is frequently decreased in glioblastoma (GBM) of the classical subtype, which possesses signature amplification or mutational activation of the epidermal growth factor (EGF) receptor. We tested the correlation bet

SUBMITTER: Woerner BM 

PROVIDER: S-EPMC3262072 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature