Abstract

IntroductionMetastasis is the movement of a tumour from its original site to a secondary site. The ability of cancer cells to metastasize depends on their motility and actin-rich membrane protrusions. These protrusions and motility are regulated by Rho GTPases, including RhoG. RhoG shares a lot of homology with Rac1 and was found to be overexpressed in many tumour tissues.Material and methodsIn this paper, we studied the role of RhoG in migration and invasion of a brain tumour cell line. In order to delineate the role of RhoG, we knocked it down using siRNA. We studied its effect on migration by time lapse analysis. We also observed its effect on adhesion using an adhesion assay and staining the cells for vinculin.Results and discussionsWe found that knocking down RhoG, using siRNA, 2D random migration of SNB19 cells significantly decreased. RhoG was also found to positively regulate cell invasion and cell adhesion. This suggested an effect of RhoG on Rac. Indeed, when RhoG was knocked down, Rac activation dramatically decreased in a pull down assay. Cell adhesion phenotype showed a complete lack of focal contacts in the RhoG KnDn cells. This was mimicked in the Rac KnDn cells and rescued when Rac was overexpressed in the same cells.ConclusionThis study shows that, in glioblastoma cells, RhoG positively regulates cell adhesion, migration and invasion through the activation of Rac.

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