Research Paper Volume 12, Issue 7 pp 5675—5692

STAT5A induced LINC01198 promotes proliferation of glioma cells through stabilizing DGCR8

Cheng Tan1, *, , Yimeng Dai2, *, , Xiaoyang Liu1, , Guifang Zhao3,4, , Weiyao Wang3,4, , Jia Li1, , Ling Qi3,4, ,

  • 1 Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, P.R. China
  • 2 Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, P.R. China
  • 3 The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan 511518, P.R. China
  • 4 Department of Pathophysiology, Jilin Medical University, Jilin 132013, P.R. China
* Equal contribution

Received: November 3, 2019       Accepted: January 27, 2020       Published: April 4, 2020
How to Cite
This article has been corrected. See Correction. Aging (Albany NY). 2021; 13:17953-17954 .  PMID: 34292878

Copyright © 2020 Tan 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.


Background: LINC01198 has been suggested to be able to predict overall prognosis for glioma; however, it has been little described in glioma.

Results: It was shown that LINC01198 was markedly enriched in neoplasmic tissues relative to normal controls; and that elevated LINC01198 significantly correlated with unfavorable overall prognosis. Moreover, activation of STAT5A, identified as transcription factor (TF), can induce the expression of LINC01198. DGCR8, a kind of RNA-binding proteins (RBPs), was identified to be able to bind with LINC01198 that can stabilize the DGCR8. Five differential miRNAs with most significant difference, including miR-21-5p, miR-34-5p, miR-1246, miR-4488 and miR-494, were obtainable after silencing of DGCR8.

Conclusions: Together, the data we presented here suggested that STAT5 induced LINC01198 promotes proliferation and motility of glioma cells through stabilizing DGCR8 in glioma cells.

Methods: Expression of LINC01198 was appraised by quantitative PCR (qPCR) and in situ hybridization (ISH) in glioma clinical specimens, totaling 100 cases. Post hoc statistical analysis was conducted. In vitro, LINC01198 was stably silenced or re-expressed by transfection with lentiviral-based vectors. Chromatin-immunoprecipitation (CHIP) was applied to identify the relevant TFs that can bind with LINC01198, which was corroborated with electrophoretic mobility shift (EMSA) assay. RNA-immunoprecipitation (RIP) was used to identify the RNA-binding protein that can bind with LINC01198. Moreover, miRNA microarray was used to screen out differential miRNAs after silencing of DGCR8.


LncRNA: long-non coding RNA; qPCR: quantitative PCR; ISH: in situ hybridization; CHIP: Chromatin-immunoprecipitation; TF: transcription factor; EMSA: electrophoretic mobility shift assay; RIP: RNA-immunoprecipitation; RBP: RNA-binding protein; STAT: Signal transducers and activators of transcription; DGCR8: DiGeorge Syndrome Critical Region Gene 8; DMEM: Dulbecco’s modified Eagle’s medium; RPMI: Roswell Park Memorial Institute; MTT: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; FBS: Fetal bovine serum; GAPDH: Glyceraldehyde3-phosphate dehydrogenase; EDTA: Ethylene Diamine Tetra acetic Acid; ECL: enhanced chemiluminescence; ANOVA: analysis of variance; OS: overall survival; DFS: disease-free survival; TCGA: The Cancer Genome Atlas; CHX: Cycloheximide; kDa: kilodalton; miR-NC: miR-scramble.