The role of Myc and let-7a in glioblastoma, glucose metabolism and response to therapy

Abstract

Glioblastoma multiforme (GBM) is thought to result from an imbalance between glucose metabolism and tumor growth. The Myc oncogene and lethal-7a microRNA (let-7a miRNA) have been suggested to cooperatively regulate multiple downstream targets leading to changes in chromosome stability, gene mutations, and/or modulation of tumor growth. Here, we review the roles of Myc and let-7a in glucose metabolism and tumor growth and addresses their future potential as prognostic markers and therapeutic tools in GBM. We focus on the functions of Myc and let-7a in glucose uptake, tumor survival, proliferation, and mobility of glioma cells. In addition, we discuss how regulation of different pathways by Myc or let-7a may be useful for future GBM therapies. A large body of evidence suggests that targeting Myc and let-7a may provide a selective mechanism for the deregulation of glucose metabolic pathways in glioma cells. Indeed, Myc and let-7a are aberrantly expressed in GBM and have been linked to the regulation of cell growth and glucose metabolism in GBM. This article is part of a Special Issue entitled "Targeting alternative glucose metabolism and regulate pathways in GBM cells for future glioblastoma therapies".

Keywords: Glioblastoma; Glucose metabolism; Let-7a miRNA; Myc; Pathways; Tumor growth.