Fig. 2

Knockdown of SNHG12 restores TMZ sensitivity in TMZ-resistant cells in vitro.a qRT-PCR analysis of SNHG12 expression in sh-control, sh-SNHG12–1, sh-SNHG12–2, sh-SNHG12–3 treated TMZ-resistant cells. b CCK-8 assay analysis revealed the effect of SNHG12 knockdown on the TMZ-resistant cells after TMZ treatment at the indicated concentrations for 48 h. c Heatmaps of SNHG12-associated genes in 83 and 227 glioblastoma tissues sorted by the level of SNHG12 expression in CGGA and Rembrandt data sets. d GO analyses were performed using the SNHG12 associated genes in CGGA and Rembrandt data sets. e Western blot test of caspase-3 and PARP in TMZ-resistant cells treated with vehicle control or TMZ (200 μM) for 48 h. β-actin was used as the loading control. f Flow cytometric analysis revealing the effect of SNHG12 knockdown on the apoptosis of TMZ- resistant cells with or without TMZ treatment (200 μM, 48 h). g TUNEL analysis of SNHG12 knockdown cells or vehicle control with or without TMZ treatment (200 μM, 48 h). Scale bar = 50 μm. h Colony formation assays of SNHG12 knockdown or vehicle control TMZ-resistant cells with or without TMZ treatment (200 μM, 48 h). i Knockdown of SNHG12 decreased the levels of p-Rb, cyclin D1 but not CDK4 and CDK6 in TMZ-resistant cells. β-actin was used as the loading control. j The cell cycle distribution was analyzed by flow cytometric analysis in TMZ-resistant cells transfected with sh-ctrl or sh-SNHG12–2. Data are presented as the mean ± SEM from three independent experiments. Significant results were presented as NS non-significant, **P<0.01, ***P<0.001