Upregulation of HOTAIRM1 increases migration and invasion by glioblastoma cells.

Long noncoding RNAs (lncRNAs) promote invasion and migration by glioblastoma (GBM) cells. In this study, quantitative real-time polymerase chain reaction was used to detect expression levels of the lncRNA HOTAIRM1 in GBM tissue samples and cells. The function of HOTAIRM1 was examined using wound healing assays, transwell assays, and in vivo experiments after GBM cells were transfected with either sh-ctrl or sh-HOTAIRM1. Luciferase reporter assays and RIP assays were performed to determine the interactions between HOTAIRM1 and miR-153-5p and between miR-153-5p and SNAI2. We also used luciferase reporter assays and ChIP assays to assess the transcriptional regulation of HOTAIRM1 by SNAI2 and CDH1. HOTAIRM1 was significantly overexpressed in GBM tissues and cells. HOTAIRM1 knockdown significantly weakened the migration and invasion by GBM cells. HOTAIRM1 was found to sponge miR-153-5p, and SNAI2 is a direct target of miR-153-5p. In addition, SNAI2 was shown to force HOTAIRM1 expression through directly promoting transcription and suppressing the negative regulation of CDH1 on transcription. Our results indicate a positive feedback loop between HOTAIRM1 and SNAI2, and suggest that the lncRNA HOTAIRM1 is a potential biomarker and therapeutic target in GBM.