High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer

Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the ph...

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Veröffentlicht in:Aging (Albany, NY.) NY.), 2020-05, Vol.12 (9), p.8728-8741
Hauptverfasser: Tan, Lei, Xiao, Kanghua, Ye, Yunlin, Liang, Haitao, Chen, Mingkun, Luo, Junhang, Qin, Zike
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container_end_page 8741
container_issue 9
container_start_page 8728
container_title Aging (Albany, NY.)
container_volume 12
creator Tan, Lei
Xiao, Kanghua
Ye, Yunlin
Liang, Haitao
Chen, Mingkun
Luo, Junhang
Qin, Zike
description Arginine methyltransferase 5 (PRMT5) is involved in a variety of cancers. We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. These results suggest that PRMT5 could be used as a potential molecular marker for BUC in the future.
doi_str_mv 10.18632/aging.103198
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We used bioinformatics analysis to investigate PRMT5 overexpression in bladder urothelial cancer (BUC) and its clinical significance. We also conducted molecular biology experiments to investigate the effect of PRMT5 on the phenotype of BUC cells in vitro and in vivo. PRMT5 was found to be upregulated in BUC tissue in the Oncomine and The Cancer Genome Atlas databases. We validated the results from these databases in a cohort of BUC samples. Kaplan-Meier and Cox multivariate analyses demonstrated that PRMT5 upregulation is an independent prognostic risk factor for BUC. The in vitro and in vivo phenotypic experiments found that downregulated expression of PRMT5 in BUC cells inhibits BUC cell proliferation and aggression. In addition, gene set enrichment analysis demonstrated that PRMT5 knockdown leads to cell cycle G1/S arrest, deactivation of Akt, and mTOR phosphorylation in BUC cells. 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subjects Animals
Biomarkers, Tumor
Cell Line, Tumor
Cell Proliferation
Databases, Factual
Disease Progression
Down-Regulation
Female
G1 Phase Cell Cycle Checkpoints
Gene Expression
Humans
Male
Mice, Inbred BALB C
Mice, Nude
Protein-Arginine N-Methyltransferases - genetics
Protein-Arginine N-Methyltransferases - metabolism
Research Paper
Survival Analysis
Up-Regulation
Urinary Bladder Neoplasms - genetics
Urinary Bladder Neoplasms - metabolism
Urinary Bladder Neoplasms - mortality
Urinary Bladder Neoplasms - pathology
Xenograft Model Antitumor Assays
title High PRMT5 expression is associated with poor overall survival and tumor progression in bladder cancer
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