Fig. 2

SNHG17 up-regulation was induced by YY1. a RT-qPCR demonstrated that p53, TFIID, YY1 and STAT4 expressions were elevated in glioma tissues among 20 transcription factors predicted to affect the transcription of SNHG17 by PRPOMO database. b RT-qPCR showed that the expression of p53, TFIID, YY1 and STAT4 was knocked down in glioma cells. c RT-qPCR manifested that the expression of SNHG17 was reduced by YY1 silence. d JASPAR database presented the binding motif of YY1 and the binding region of YY1 on SNHG17 promoter. e ChIP assay demonstrated that P3 region (− 647 to − 642, GCCATG) was responsive to YY1-mediated transcription of SHNG17. f Luciferase reporter assay illustrated that YY1 could bind with SNHG17 promoter. g RT-qPCR displayed the expression of YY1 in glioma cells. h RT-qPCR showed the expression of SNHG17. i RT-qPCR examined the SNHG17 expression. j–l CCK-8, colony formation and EdU assays revealed that cell proliferative capacity was hampered by YY1 depletion and was promoted by overexpression of SNHG17. m, n Flow cytometry and TUNEL assays unveiled that enhanced cell apoptosis by silence of YY1 was reversed by SNHG17 up-regulation. o Western blot assay demonstrated that increased protein level of cleaved-caspase3, cleaved-caspase9 and Bax by YY1 ablation was rescued by SNHG17 enhancement. **P < 0.01