Research Paper Volume 13, Issue 2 pp 2348—2364

Upregulation of HOTAIRM1 increases migration and invasion by glioblastoma cells

SNAI2 transcriptionally regulates HOTAIRM1 in GBM cells. (A) Two potential SNAI2-binding sites in the HOTAIRM1 promoter region were predicted using the high-quality transcription factor binding profile database (JASPAR). (B) The two predicted regions were transcriptionally responsive to SNAI2 overexpression, as shown in luciferase reporter assays. (C) Wild-type or mutant luciferase reporter were transfected into GBM cells, and the luciferase reporter activity were analyzed. (D) SNAI2 bound to both predicted binding sites in HOTAIRM1 promoter, as shown in ChIP assays. (E) SNAI2 shRNA reduced the levels of HOTAIRM1 in U251 and pGBM1 cells, as shown in qRT-PCR analysis (top) and western blotting (bottom).

Figure 5. SNAI2 transcriptionally regulates HOTAIRM1 in GBM cells. (A) Two potential SNAI2-binding sites in the HOTAIRM1 promoter region were predicted using the high-quality transcription factor binding profile database (JASPAR). (B) The two predicted regions were transcriptionally responsive to SNAI2 overexpression, as shown in luciferase reporter assays. (C) Wild-type or mutant luciferase reporter were transfected into GBM cells, and the luciferase reporter activity were analyzed. (D) SNAI2 bound to both predicted binding sites in HOTAIRM1 promoter, as shown in ChIP assays. (E) SNAI2 shRNA reduced the levels of HOTAIRM1 in U251 and pGBM1 cells, as shown in qRT-PCR analysis (top) and western blotting (bottom).