Research Paper Volume 13, Issue 2 pp 2348—2364
Upregulation of HOTAIRM1 increases migration and invasion by glioblastoma cells
- 1 Department of Neurosurgery, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
- 2 Department of Oncology, Huaian Hospital of Huaian District, Huai’an, Jiangsu Province, China
- 3 Department of Central Laboratory, The Affiliated Huai’an No.1 People's Hospital of Nanjing Medical University, Huai’an, Jiangsu Province, China
- 4 Department of Neurology, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
- 5 Department of Intensive Care Unit, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
- 6 Department of Image, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
- 7 Department of Neurosurgery, First Affiliated Hospital of Soochow University, Suzhou, China
- 8 Galactophore Department, Jiangsu Huai’an Maternity and Children Hospital, Huai'an, Jiangsu Province, China
Received: January 13, 2020 Accepted: September 18, 2020 Published: December 11, 2020
https://doi.org/10.18632/aging.202263How to Cite
Copyright: © 2020 Xie et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
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.