Protein Kinase CK2 Content in GL261 Mouse Glioblastoma
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Glioblastoma (GBM) is the most prevalent and aggressive human glial tumour with a median survival of 14–15 months. Temozolomide (TMZ) is the standard chemotherapeutic choice for GBM treatment. Unfortunately, chemoresistence always ensues with concomitant tumour regrowth. Protein kinase CK2 (CK2) contributes to tumour development, proliferation, and suppression of apoptosis in cancer and it is overexpressed in human GBM. Targeting CK2 in GBM treatment may benefit patients. With this translational perspective in mind, we have studied the CK2 expression level by Western blot analysis in a preclinical model of GBM: GL261 cells growing orthotopically in C57BL/6 mice. The expression level of the CK2 catalytic subunit (CK2α) was higher in tumour (about 4-fold) and in contralateral brain parenchyma (more than 2-fold) than in normal brain parenchyma (p < 0.05). In contrast, no significant changes were found in CK2 regulatory subunit (CK2β) expression, suggesting an increased unbalance of CK2α/CK2β in GL261 tumours with respect to normal brain parenchyma, in agreement with a differential role of these two subunits in tumours.
KeywordsGlioma CK2 content Preclinical brain tumor GBM therapeutic targets
Protein kinase CK2
This work was supported by: SAF 2011-23870, SAF2014-52332-R, SGR191-2014 and Centro de Investigación Biomédica en Red – Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN, [http://www.ciber-bbn.es/en]), an initiative of the Instituto de Salud Carlos III (Spain) co-funded by EU FEDER funds.
Conflict of interest diclosures
The authors have no financial conflicts to disclose.
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