Histone deacetylase 3 implicated in the pathogenesis of children glioma by promoting glioma cell proliferation and migration

• HDAC3 was significantly elevated in children's gliomas.
• High HDAC3 expression was correlated with a poor prognosis of children with glioma.
• Inhibition of HDAC3 suppressed proliferation and migration of glioma cells.
• Inhibition of HDAC3 induced G0/G1 arrest and apoptosis of glioma cells.

BackgroundGlioma is an aggressive cancer with high mortality, especially in children. It is known that histone modification plays an important role in the pathogenesis of various cancers. However, it is unknown whether histone deacetylase 3 (HDAC3) plays a role in the tumorigenesis of children gliomas. This study was aimed to explore the potential effects of HDAC3 in children gliomas. Expression of HDAC3 was measured in children glioma samples (n=70) and normal brain tissues (n=7) by real-time PCR and western blotting. Survival of the two groups was analyzed by the Kaplan–Meier method. The effects of HDAC3 in the pathogenesis of gliomas were analyzed by silencing the glioma cells U87-MG and U251. Data showed that HDAC3 was significantly elevated in children's gliomas, following the glioma grade, with almost no expression in normal brain tissues. Ectopic HDAC3 expression was correlated with poorer prognosis of children with glioma. In glioma cell lines, inhibition of HDAC3 using siRNA could suppress proliferation and sphere formation, induce G0/G1 arrest and apoptosis, and suppress the migration of glioma cells in comparison with controls. The higher level of HDAC3 expression was associated with more advanced tumor grades and shorter survival. HDAC3 participated in the pathogenesis of children gliomas by promoting glioma cell proliferation and migration.