The Role of Palladin in the Regulation of A172 Glioblastoma Cell Adhesion and Invasion through its Crosstalk with RhoGTPases

Abstract

Classified as a grade IV neoplasm, Glioblastoma multiform (GBM) is considered a highly lethal and malignant tumor of the brain and the central nervous system (CNS). This cancer might arise with a benign nature which will lead to its localization to the primary tumor site. However, it might progress, develop, and metastasize to distinct regions of the body. For this to occur, GBMs will be relying on different cellular processes that will ensure the remodeling of its actin cytoskeleton providing the cells with movement abilities, by regulating cell adhesion, cell invasion, and invadopodia formation. Palladin is a novel phosphoprotein, discovered recently as a scaffold regulator of the actin filaments through its binding with its partners and via its crosstalk with RhoGTPases. Our study investigated the role presented by Palladin in modulating these cellular processes in GBMs, by its control over the rearrangement of actin bundles as well as its interplay with RhoGTPases. The findings of this research suggested that Palladin is a positive regulator of GBM cell adhesion through its effect on RhoA expression. In addition, this protein was also found to be a negative modulator of cell invasion in this tumor via controlling the formation of invadopodia structures mediating this mechanism.