Fig. 6: PANDAR depletion combined with nutlin-3 synergistically inhibited proliferation and induced apoptosis in GC cells. | Cell Death & Disease

Fig. 6: PANDAR depletion combined with nutlin-3 synergistically inhibited proliferation and induced apoptosis in GC cells.

From: Long noncoding RNA PANDAR blocks CDKN1A gene transcription by competitive interaction with p53 protein in gastric cancer

Fig. 6

a After treated with nutlin-3 (10 μm) and ADM (0.2 mg/ml) for 4 h, PANDAR-depleted AGS cells were analysed by immunoblot analysis. WT, wild type; −/−, knockout. b After treated with nutlin-3 and ADM for 4 h, PANDAR-depleted AGS cells were analysed by flow cytometry analysis. c The effect of PANDAR on affecting AGS cells to ADM-induced apoptosis. d Immunoblotting analysis determined the p53 and p21 protein levels of AGS cells treated with CRISPR/Cas9 system for PANDAR and nutlin-3 (10 µm) for 72 h. e Xenografts treated with nutlin-3 via oral administration at 200 mg/kg once daily for 6 weeks. IHC analysis determined the p21 protein levels in tumour tissues. f The presence of apoptotic cells in the representative tumour tissues was detected by a TUNEL assay. g Anti-tumour effect of PANDAR depleting combined with nutlin-3. The bar graph shows the average tumour weight per mouse and the standard deviation. h Stable PANDAR-depleted AGS cells were injected into immunodeficient mice (three animals per group) by tail vein assays and subsequently received 200 mg/kg of an oral dose of nutlin-3 once daily. After 2 weeks, nude mice were evaluated for lung colonization capacity. i A model illustrating the putative roles of PANDAR in controlling the transcription of CDKN1A gene through competitive binding with p53 protein

Back to article page