Up-Regulation of the Alpha Prime Subunit of Protein Kinase CK2 as a Marker of Fast Proliferation in GL261 Cultured Cells

Abstract

Glioblastoma (GB) is the most prevalent malignant primary brain tumor in adults. The preclinical glioblastoma model GL261 is widely used for investigating new therapeutic strategies. GL261 cultured cells are used for assessing preliminary in vitro data for this model although very little is known about the molecular characteristics of this cell line. Protein Kinase CK2 is a pleiotropic serine-threonine kinase and its inhibition may be a promising therapeutic strategy for GB treatment. In our group we follow treatment response with CK2 inhibitors in vivo using the GL261 murine model. For that, it is of our interest to assess the differential expression of α, α', β CK2 subunits as well as CK2 activity in the GL261 GB model. CK2α' expression changed along the growth curve of GL261 cells, undergoing downregulation in postconfluent phase cells, whereas CK2α and CK2β expression remained essentially unchanged. Furthermore, a marked decrease in CK2 activity in slowly proliferating postconfluent phase GL261 cells was observed. Finally, CK2α' expression in orthotopic GL261 tumors was intermediate between CK2α' expression found in cultured cells in exponentially growing or postconfluent phase, reflecting the heterogeneous nature of GL261 tumours growing in vivo. The results obtained suggest that, in the GL261 cell line, CK2α' could play a specific role in highly proliferative cells. Also, the decrease in CK2 activity in slowly proliferating GL261 cells could imply a differential susceptibility to subunit-specific CK2 inhibitors in this cell line, although further studies are needed to confirm this hypothesis.

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