Furthermore, a nestin downregulation is associated with an increased adhesion to collagen, bronectin, and laminin, leading to an inhibition of migration of glioma cells, while overexpression had the reverse eect. This might be of further interest, as nestin was especially found in cells at the invasive front of glioma. The underlying molecular mechanisms of these nestin induced eects remained unclear so far.It remains tempting to speculate that, in glioma, a similar mechanism as discussed before might be Acalabrutinib responsible for the increased migratory capacity, via an activation of FAK and regulation of integrin localization. The intermediate lament synemin seems to be an additional part of the motile machinery of astrocytoma cells.Nevertheless, precise mechanisms of synemin actions in glioma are missing.Intermediate laments are not only dierentially expressed in glioma, but III, IV, and tubulin are also overexpressed in glioma. Notably, taxol was suggested to trigger dierentiation in some glioma cells and in one study associated with an increase in GFAP expression. The higher expression of tubulin might be related to centrosome abnormalities, altered microtubule dynamics, and consequently, adhesion dynamics and cell polarization. Furthermore, the microtubule severing Dabigatran protein spastin and the destabilizing protein stathmin are both associated with increased motility and, in case of spastin, also with reduced proliferation. Spastin expression is increased in glioma and mainly located at the cell front and the mitotic spindle, implying an indirect role in both motility and cell division by destabilization of microtubules, inducing spindle formation defects during division and facilitating microtubule turnover at the front to adapt to changes of the microenvironment.For the microtubule associated protein DCX dierent, contradictory results were found.Few studies reported that DCX is preferentially expressed at the invasive front of glioma, indicating a proinvasive role.Other authors demonstrated a very low DCX expression in glioma and that a forced expression causes apoptosis and inhibits invasion. Accordingly, the role of DCX in glioma needs to be critically evaluated.In contrast, the role of EB seems to be unambiguous, the reduced accumulation of EB at microtubule tips is associated with higher microtubule instability, a less migratory and motile phenotype of glioma cells, caused by a lower amount of microtubules reaching the leading edge. The microtubule stabilizing factor APC, despite regulating dierentiation and cell cycle arrest, might also be part of the migratory machinery of glioma cells, as it was recently shown that vimentin, GFAP, and nestin organization, along microtubules in the glioblastoma cell line UMG, is critically dependent on APC. APC may, additionally, increase the vimentin polymerization rate and, thus, inuence migration. The motor protein dynein is not dierentially expressed in glioma cells in general, but migrating glioma cells express increased amounts of the protein. Dynein is, in part, responsible for microtubule dependent intracellular transport and it can be speculated that dynein is necessary to maintain cell polarization by transporting inhibitory signals away from the cell front. Summary of motility associated proteins dierentially expressed in glioma, compared to healthy glia cells.The idea of such a mechanism is supported by the observed drop in glioma migration after inhibition of or vintegrin and increased motility after overexpression.