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Plos One : Targeting Gastrin-releasing Peptide Suppresses Neuroblastoma Progression Via Upregulation of Pten Signaling, Volume 8

By Rota, Rossella

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Book Id: WPLBN0003967487
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Targeting Gastrin-releasing Peptide Suppresses Neuroblastoma Progression Via Upregulation of Pten Signaling, Volume 8  
Author: Rota, Rossella
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Rota, R. (n.d.). Plos One : Targeting Gastrin-releasing Peptide Suppresses Neuroblastoma Progression Via Upregulation of Pten Signaling, Volume 8. Retrieved from http://netlibrary.net/


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Description : We have previously demonstrated the role of gastrin-releasing peptide (GRP) as an autocrine growth factor for neuroblastoma. Here, we report that GRP silencing regulates cell signaling involved in the invasion-metastasis cascade. Using a doxycycline inducible system, we demonstrate that GRP silencing decreased anchorage-independent growth, inhibited migration and neuroblastoma cell-mediated angiogenesis in vitro, and suppressed metastasis in vivo. Targeted inhibition of GRP decreased the mRNA levels of oncogenes responsible for neuroblastoma progression. We also identified PTEN/AKT signaling as a key mediator of the tumorigenic properties of GRP in neuroblastoma cells. Interestingly, PTEN overexpression decreased GRP-mediated migration and angiogenesis: a novel role for this, otherwise, understated tumor suppressor in neuroblastoma. Furthermore, activation of AKT (pAKT) positively correlated with neuroblastoma progression in an in vivo tumor-metastasis model. PTEN expression was slightly decreased in metastatic lesions. A similar phenomenon was observed in human neuroblastoma sections, where, early-stage localized tumors had a higher PTEN expression relative to pAKT: however, an inverse expression pattern was observed in liver lesions. Taken together, our results argue for a dual purpose of targeting GRP in neuroblastoma –1) decreasing expression of critical oncogenes involved in tumor progression, and 2) enhancing activation of tumor suppressor genes to treat aggressive, advanced-stage disease.

 

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