The knocking down of the oncoprotein Golgi phosphoprotein 3 in T98G cells of glioblastoma multiforme disrupts cell migration by affecting focal adhesion dynamics in a focal adhesion kinase-dependent manner.

摘要: Golgi phosphoprotein 3 (GOLPH3) is a conserved protein of the apparatus that in humans has been implicated tumorigenesis. However, precise function GOLPH3 malignant transformation still unknown. Nevertheless, clinicopathological data shows more than dozen kinds cancer, including gliomas, could be found overexpressed, which correlates with poor prognosis. Experimental overexpression leads to primary cells and tumor growth enhancement. Conversely, knocking down GOLPH3-overexpressing reduces tumorigenic features, such as cell proliferation migration invasion. The cumulative evidence indicate an oncoprotein promotes tumorigenicity by mechanism impact at different levels types cells, sorting glycosyltransferases, signaling pathways, actin cytoskeleton. How connects mechanistically these processes not determined yet. Further studies are important have complete understanding role oncoprotein. Given genetic diversity outstanding aspect how this inherent heterogeneity possibly exert its oncogenic function. We aimed evaluate contribution phenotype cells. Here, we analyzed effect on resulted from stable, RNAi-mediated T98G glioblastoma multiforme, human glioma line unique features. reduction produced dramatic changes morphology, involving rearrangements cytoskeleton number dynamics focal adhesions. These effects correlated decreased invasion due affected persistence directionality motility. Moreover, also caused autoactivation adhesion kinase (FAK), cytoplasmic tyrosine regulates Our support model stimulating activity FAK.