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Research Paper|Volume 13, Issue 2|pp 2348—2364

Upregulation of HOTAIRM1 increases migration and invasion by glioblastoma cells

Peng Xie1, Xiang Li2,3, Rui Chen4, Yue Liu5, DaChao Liu6, Wenguang Liu1, Gang Cui7, Jinjing Xu8
  • 1Department of Neurosurgery, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
  • 2Department of Oncology, Huaian Hospital of Huaian District, Huai’an, Jiangsu Province, China
  • 3Department of Central Laboratory, The Affiliated Huai’an No.1 People's Hospital of Nanjing Medical University, Huai’an, Jiangsu Province, China
  • 4Department of Neurology, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
  • 5Department 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
  • 6Department of Image, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai'an, Huai’an, Jiangsu Province, China
  • 7Department of Neurosurgery, First Affiliated Hospital of Soochow University, Suzhou, China
  • 8Galactophore Department, Jiangsu Huai’an Maternity and Children Hospital, Huai'an, Jiangsu Province, China
* Equal contribution
Received: January 13, 2020Accepted: September 18, 2020Published: December 11, 2020
https://doi.org/10.18632/aging.202263

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.