Glioblastoma is the most common and malignant type of
primary brain tumor. Previous studies have shown that alterations in centrosome amplification and its components are frequently found in treatment-resistant
tumors and may be associated with
tumor progression. A centrosome
protein essential for centrosome biogenesis is the centromere
protein J (CENPJ), known to control the proliferation of neural progenitors and hepatocarcinoma cells, and also neuronal migration. However, it remains unknown the role of CENPJ in
glioblastoma. Here we show that CENPJ is overexpressed in human
glioblastoma cell lines in comparison to human astrocytes. Using bioinformatics analysis, we find that high Cenpj expression is associated with poor prognosis in
glioma patients. Examining Cenpj loss of function in
glioblastoma by
siRNA transfection, we find impairments in cell proliferation and migration. Using a Cenpj mutant version with the deleted PN2-3 or TCP domain, we found that a conserved PN2-3 region is required for
glioblastoma migration. Moreover, Cenpj downregulation modulates
glioblastoma morphology resulting in microtubules stabilization and actin filaments depolymerization. Altogether, our findings indicate that CENPJ controls relevant aspects of
glioblastoma progression and might be a target for therapeutic intervention and a
biomarker for
glioma malignancy.