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BioMed Research International
Volume 2017 (2017), Article ID 7082696, 14 pages
https://doi.org/10.1155/2017/7082696
Review Article

mTOR-Dependent Cell Proliferation in the Brain

1Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy
2I.R.C.C.S. Neuromed, Via Atinense 18, Pozzilli, 86077 Isernia, Italy

Correspondence should be addressed to Francesco Fornai; ti.ipinu.dem@ianrof.ocsecnarf

Received 17 July 2017; Accepted 22 October 2017; Published 13 November 2017

Academic Editor: Marta M. Alonso

Copyright © 2017 Larisa Ryskalin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The mammalian Target of Rapamycin (mTOR) is a molecular complex equipped with kinase activity which controls cell viability being key in the PI3K/PTEN/Akt pathway. mTOR acts by integrating a number of environmental stimuli to regulate cell growth, proliferation, autophagy, and protein synthesis. These effects are based on the modulation of different metabolic pathways. Upregulation of mTOR associates with various pathological conditions, such as obesity, neurodegeneration, and brain tumors. This is the case of high-grade gliomas with a high propensity to proliferation and tissue invasion. Glioblastoma Multiforme (GBM) is a WHO grade IV malignant, aggressive, and lethal glioma. To date, a few treatments are available although the outcome of GBM patients remains poor. Experimental and pathological findings suggest that mTOR upregulation plays a major role in determining an aggressive phenotype, thus determining relapse and chemoresistance. Among several activities, mTOR-induced autophagy suppression is key in GBM malignancy. In this article, we discuss recent evidence about mTOR signaling and its role in normal brain development and pathological conditions, with a special emphasis on its role in GBM.