Open AccessOverview of the molecular mechanisms of migration and invasion in glioblastoma multiforme
Author(s) -
Xian Liu,
Ju Yu Chen,
Yueh Chien,
Yi Yang,
Ming Teh Chen,
Liang Yu Lin
Publication year - 2021
Publication title -
journal of the chinese medical association
Language(s) - English
Resource type - Journals
eISSN - 1728-7731
pISSN - 1726-4901
DOI - 10.1097/jcma.0000000000000552
Subject(s) - extracellular matrix , protein kinase b , signal transduction , microrna , medicine , motility , cancer research , competing endogenous rna , cell migration , glioblastoma , phenotype , neuroscience , biology , rna , cell , microbiology and biotechnology , gene , long non coding rna , genetics
Glioblastoma (GBM) is one of the most devastating cancers, with an approximate median survival of only 16 months. Although some new insights into the fantastic heterogeneity of this kind of brain tumor have been revealed in recent studies, all subclasses of GBM still demonstrate highly aggressive invasion properties to the surrounding parenchyma. This behavior has become the main obstruction to current curative therapies as invasive GBM cells migrate away from these foci after surgical therapies. Therefore, this review aimed to provide a relatively comprehensive study of GBM invasion mechanisms, which contains an intricate network of interactions and signaling pathways with the extracellular matrix (ECM). Among these related molecules, TGF-β, the ECM, Akt, and microRNAs are most significant in terms of cellular procedures related to GBM motility and invasion. Moreover, we also review data indicating that Musashi-1 (MSI1), a neural RNA-binding protein (RBP), regulates GBM motility and invasion, maintains stem cell populations in GBM, and promotes drug-resistant GBM phenotypes by stimulating necessary oncogenic signaling pathways through binding and regulating mRNA stability. Importantly, these necessary oncogenic signaling pathways have a close connection with TGF-β, ECM, and Akt. Thus, it appears promising to find MSI-specific inhibitors or RNA interference-based treatments to prevent the actions of these molecules despite using RBPs, which are known as hard therapeutic targets. In summary, this review aims to provide a better understanding of these signaling pathways to help in developing novel therapeutic approaches with better outcomes in preclinical studies.