U251 and U87 cells were seeded in 24-well plates at a density of 1 × 105 cells/well and maintained for 24 h at 37°C. Small-interfering RNAs (siRNAs) targeting FGD5-AS1 (si-FGD5-AS1-1 and si-FGD5-AS1-2) and the corresponding negative control (si-NC) were obtained from GenePharma Co., Ltd (Shanghai, China). An overexpression plasmid of miR-103a-3p (miR-103a-3p) and negative control (miR-NC) as well as an miR-103a-3p inhibitor (miR inhibitor) and a negative control (inhibitor-NC) were obtained from GenePharma. U251 and U87 cells were infected with the oligonucleotides stated above using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). Cells without transfection were regarded as the blank group. To investigate the interaction between FGD5-AS1-1 and miR-103a-3p, U251 and U87 cells were co-transfected with si-FGD5-AS1 or si-NC and miR inhibitor or inhibitor-NC using Lipofectamine 2000.
pcDNA-TPD52 (TPD52) and negative control (pcDNA-NC) were purchased from GenePharma. To explore whether TPD52 was involved in the role of FGD5-AS1 in GBM, U251 cells were co-transfected with si-FGD5-AS1 or si-NC and pcDNA-NC or pcDNA-TPD52 using Lipofectamine 2000. Cells were analyzed after 48 h of transfection.
pcDNA-TPD52 (TPD52) and negative control (pcDNA-NC) were purchased from GenePharma. To explore whether TPD52 was involved in the role of FGD5-AS1 in GBM, U251 cells were co-transfected with si-FGD5-AS1 or si-NC and pcDNA-NC or pcDNA-TPD52 using Lipofectamine 2000. Cells were analyzed after 48 h of transfection.