title: 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".
authors.affiliation: Department of Pharmaceutics, Shanghai Eighth People's Hospital, Shanghai 200235, China; Hubei University of Medicine, No. 30 People South Road, Shiyan City, Hubei Province 442000, China. Electronic address: wangan139@163.com.
authors.forename: Gang
authors.initials: G
authors.lastname: Wang
authors.affiliation: Department of Pharmaceutics, Shanghai Eighth People's Hospital, Shanghai 200235, China; Hubei University of Medicine, No. 30 People South Road, Shiyan City, Hubei Province 442000, China.
authors.forename: JunJie
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region.
authors.forename: HuaFu
authors.initials: H
authors.lastname: Zhao
authors.affiliation: Department of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region.
authors.forename: Shing Shun
authors.initials: SS
authors.lastname: Tony To
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic; D042822:Genomic Instability; D005909:Glioblastoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D005947:Glucose / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; C489427:MYC protein, human; D035683:MicroRNAs; D016271:Proto-Oncogene Proteins c-myc; C487931:mirnlet7 microRNA, human; D005947:Glucose
keywords: Glioblastoma; Glucose metabolism; Let-7a miRNA; Myc; Pathways; Tumor growth