====== Glioblastoma invasion mechanism ======

Contains an intricate network of interactions and [[signaling pathway]]s with the [[extracellular matrix]]. Among these related [[molecule]]s, [[TGF-β]], the [[ECM]], [[Akt]], and [[microRNA]]s are most significant in terms of cellular procedures related to [[Glioblastoma motility]] and [[invasion]]. [[Musashi-1]] ([[MSI1]]), a neural [[RNA-binding protein]] (RBP), regulates Glioblastoma motility and invasion, maintains stem cell populations in Glioblastoma, and promotes drug-resistant Glioblastoma 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.
((Liu X, Chen JY, Chien Y, Yang YP, Chen MT, Lin LT. Overview of the Molecular Mechanisms of Migration and Invasion in Glioblastoma Multiforme. J Chin Med Assoc. 2021 May 21. doi: 10.1097/JCMA.0000000000000552. Epub ahead of print. PMID: 34029218.)).