To analyze the effects of beta-transducin repeat-containing proteins (β-TrCP1) and herpes associated ubiquitin specific proteas (HAUSP) on proliferation and invasion abilities of glioblastoma cells, as well as the expression of epigenetic factor UHRF1.

The U87 glioblastoma cells were respectively transfected with blank N1 plasmid (NC) and N1 plasmid containing β-TrCP1 coding sequence (β-TrCP1), as well as control oligonucleotides (si-NC) and siRNAs targeting HAUSP mRNA (si-HAUSP). The mRNA and protein levels of β-TrCP1, HAUSP and UHRF1 were detected by RT-qPCR and Western blot, respectively. The proliferation and invasion abilities of each group cells were detected by CCK8 and Matrigel-transwell invasive assay, respectively.

Post-transfection of plasmids, the proliferation abilities of β-TrCP1 group cells were markedly decreased compared with those of NC groups cells at the fourth and the fifth day post-transfection (all P<0.05). The number of invased cells of β-TrCP1 group was significantly lower than that of NC group at the fourth day post-transfection (P< 0.05). On the other hand, post-transfection of siRNAs, the proliferation abilities of si-HAUSP group cells were significantly decreased compared with those of si-NC groups cells at the fourth and the fifth day post-transfection (P<0.05). The number of invasive cells of si-HAUSP group was significantly lower than that of si-NC group at the fourth day post-transfection (P<0.05). Furthermore, the protein level of UHRF1 was markedly downregulated by β-TrCP1 overexpression or HAUSP knockdown (all P<0.05), but the mRNA level was not affected (all P>0.05).

Both the proliferation and invasion abilities of glioblastoma U87 cells, as well the UHRF1 protein level, could be inhibited by β-TrCP1 overexpression or HAUSP knockdown. The affection of β-TrCP1 and HAUSP on proliferation and invasion abilities of GBM is probably mediated by the protein level change of UHRF1.