Research Paper Volume 11, Issue 19 pp 8156—8168

Knockdown of CREB3 activates endoplasmic reticulum stress and induces apoptosis in glioblastoma

Figure 3. The upregulation of CREB3 promoted the proliferation of SHG-44 cells. (A) The relative levels of CREB3 in four cell lines (HA1800, SHG-44, U251MG and U87MG cells) were detected by qRT-PCR. (B, C) The relative levels of CREB3 in HA1800, SHG-44, U251MG and U87MG cells were detected by Western blotting. β-actin was used as a loading control. (D) CREB3 levels in SHG-44 cells transfected with the NC or lenti-CREB3 were detected by qRT-PCR. (E, F) CREB3 levels in SHG-44 cells transfected with the NC or lenti-CREB3 were measured by Western blotting. β-actin was used as a loading control. (G) The viability of SHG-44 cells transfected with the NC or lenti-CREB3 was detected with a CCK-8 assay at 0, 24, 48 and 72 h. (H, I) The relative fluorescence levels were quantified for KI67 and DAPI staining. *P<0.05, **P<0.01 compared with the HA1800 group or NC group.