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The RNA polymerase II subunit B (RPB2) functions as a growth regulator in human glioblastoma.

Authors :
Li XL
Xie Y
Chen YL
Zhang ZM
Tao YF
Li G
Wu D
Wang HR
Zhuo R
Pan JJ
Yu JJ
Jia SQ
Zhang Z
Feng CX
Wang JW
Fang F
Qian GH
Lu J
Hu SY
Li ZH
Pan J
Source :
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2023 Sep 24; Vol. 674, pp. 170-182. Date of Electronic Publication: 2023 Jun 29.
Publication Year :
2023

Abstract

Glioblastoma multiforme (GBM) is the most common and aggressive brain tumor with a poor prognosis. The growth of GBM cells depends on the core transcriptional apparatus, thus rendering RNA polymerase (RNA pol) complex as a candidate therapeutic target. The RNA pol II subunit B (POLR2B) gene encodes the second largest subunit of the RNA pol II (RPB2); however, its genomic status and function in GBM remain unclear. Certain GBM data sets in cBioPortal were used for investigating the genomic status and expression of POLR2B in GBM. The function of RPB2 was analyzed following knockdown of POLR2B expression by shRNA in GBM cells. The cell counting kit-8 assay and PI staining were used for cell proliferation and cell cycle analysis. A xenograft mouse model was established to analyze the function of RPB2 in vivo. RNA sequencing was performed to analyze the RPB2-regulated genes. GO and GSEA analyses were applied to investigate the RPB2-regulated gene function and associated pathways. In the present study, the genomic alteration and overexpression of the POLR2B gene was described in glioblastoma. The data indicated that knockdown of POLR2B expression suppressed tumor cell growth of glioblastoma in vitro and in vivo. The analysis further demonstrated the identification of the RPB2-regulated gene sets and highlighted the DNA damage-inducible transcript 4 gene as the downstream target of the POLR2B gene. The present study provides evidence indicating that RPB2 functions as a growth regulator in glioblastoma and could be used as a potential therapeutic target for the treatment of this disease.<br />Competing Interests: Declaration of competing interest The authors have declared that no competing interest exists.<br /> (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1090-2104
Volume :
674
Database :
MEDLINE
Journal :
Biochemical and biophysical research communications
Publication Type :
Academic Journal
Accession number :
37423037
Full Text :
https://doi.org/10.1016/j.bbrc.2023.06.088