The novel tumor suppressor NOL7 post-transcriptionally regulates thrombospondin-1 expression. Publique Deposited
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MLA citation styleNature Publishing Group. 2013. https://mushare.marian.edu/concern/generic_works/7ccc118d-7216-48b9-8acf-c23076895a8c?locale=fr The Novel Tumor Suppressor Nol7 Post-transcriptionally Regulates Thrombospondin-1 Expression.
APA citation style(2013). The novel tumor suppressor NOL7 post-transcriptionally regulates thrombospondin-1 expression. https://mushare.marian.edu/concern/generic_works/7ccc118d-7216-48b9-8acf-c23076895a8c?locale=fr
Chicago citation styleThe Novel Tumor Suppressor Nol7 Post-Transcriptionally Regulates Thrombospondin-1 Expression. Nature Publishing Group. 2013. https://mushare.marian.edu/concern/generic_works/7ccc118d-7216-48b9-8acf-c23076895a8c?locale=fr
Note: These citations are programmatically generated and may be incomplete.
Thrombospondin-1 (TSP-1) is an endogenous inhibitor of angiogenesis whose expression suppresses tumor growth in vivo. Like many angiogenesis-related genes, TSP-1 expression is tightly controlled by various mechanisms, but there is little data regarding the contribution of post-transcriptional processing to this regulation. NOL7 is a novel tumor suppressor that induces an antiangiogenic phenotype and suppresses tumor growth, in part through upregulation of TSP-1. Here we demonstrate that NOL7 is an mRNA-binding protein that must localize to the nucleoplasm to exert its antiangiogenic and tumor suppressive effects. There, it associates with the RNA-processing machinery and specifically interacts with TSP-1 mRNA through its 3'UTR. Reintroduction of NOL7 into SiHa cells increases luciferase expression through interaction with the TSP-1 3'UTR at both the mRNA and protein levels. NOL7 also increases endogenous TSP-1 mRNA half-life. Further, NOL7 post-transcriptional stabilization is observed in a subset of angiogenesis-related mRNAs, suggesting that the stabilization of TSP-1 may be part of a larger novel mechanism. These data demonstrate that NOL7 significantly alters TSP-1 expression and may be a master regulator that coordinates the post-transcriptional expression of key signaling factors critical for the regulation of the angiogenic phenotype.
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