Long non-coding RNA CASP5 promotes the malignant phenotypes of human glioblastoma multiforme

Biochem Biophys Res Commun. 2018 Jun 12;500(4):966-972. doi: 10.1016/j.bbrc.2018.04.217. Epub 2018 May 2.

Abstract

Background: Long non-coding RNAs (lncRNAs) have been demonstrated to be intensively involved in the development of various carcinomas, including glioblastoma multiforme (GBM). However, only a few of them have been well characterized. LncRNA CASP5 have been found to be up-regulated in GBM tissues compared with normal tissues in a microarray-based lncRNA profiling study. In the present study, we further explored the biological role of lncRNA CASP5 in GBM.

Methods: We examined the expression level of lncRNA CASP5 in GBM tissues as well as GBM cell lines. CCK-8 assay, flow cytometric analysis, western blotting, orthotopic GBM model as well as transwell assay were performed to investigate the biological role of CASP5.

Results: We observed that lncRNA CASP5 was highly expressed in GBM tissues and cell lines. Knockdown of CASP5 greatly inhibited GBM proliferation and resulted in G1 cell cycle arrest along with higher apoptosis ratios in vitro and in vivo, while overexpression led to the opposite phenomenon. Furthermore, the migration and invasion ability of GBM cells were significantly decreased after CASP5 down-regulation, while increased migration and invasion can be observed after CASP5 up-regulation.

Conclusion: We demonstrate for the first time the potential oncogenic role of lncRNA CASP5 which may be helpful for identifying novel therapeutic targets in GBM.

Keywords: GBM; Invasion; Proliferation; lncRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antagomirs / genetics
  • Antagomirs / metabolism
  • Apoptosis / genetics
  • Brain Neoplasms / genetics*
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / pathology
  • Brain Neoplasms / therapy
  • Caspases / genetics*
  • Caspases / metabolism
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • G1 Phase Cell Cycle Checkpoints / genetics*
  • Gene Expression Regulation, Neoplastic*
  • Genes, Reporter
  • Glioblastoma / genetics*
  • Glioblastoma / metabolism
  • Glioblastoma / pathology
  • Glioblastoma / therapy
  • Humans
  • Luciferases / genetics
  • Luciferases / metabolism
  • Male
  • Mice
  • Mice, Nude
  • Oligoribonucleotides / genetics
  • Oligoribonucleotides / metabolism
  • Plasmids / chemistry
  • Plasmids / metabolism
  • RNA, Long Noncoding / agonists
  • RNA, Long Noncoding / antagonists & inhibitors
  • RNA, Long Noncoding / genetics*
  • RNA, Long Noncoding / metabolism
  • Signal Transduction
  • Stereotaxic Techniques
  • Transfection
  • Xenograft Model Antitumor Assays

Substances

  • Antagomirs
  • Oligoribonucleotides
  • RNA, Long Noncoding
  • Luciferases
  • CASP5 protein, human
  • Caspases