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pmid:32702667

RPP30, a transcriptional regulator, is a potential pathogenic factor in glioblastoma.

Guanzhang Li · You Zhai · Hanjie Liu · Zhiliang Wang · Ruoyu Huang · Haoyu Jiang · Yuemei Feng · Yuanhao Chang · Fan Wu · Fan Zeng · Tao Jiang · Wei Zhang

Aging · 2020 doi:10.18632/aging.103596

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:32702667
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science-record
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title
RPP30, a transcriptional regulator, is a potential pathogenic factor in glioblastoma.
doi
10.18632/aging.103596
pmid
32702667
authors array · 12 items
[0]
Guanzhang Li
[1]
You Zhai
[2]
Hanjie Liu
[3]
Zhiliang Wang
[4]
Ruoyu Huang
[5]
Haoyu Jiang
[6]
Yuemei Feng
[7]
Yuanhao Chang
[8]
Fan Wu
[9]
Fan Zeng
[10]
Tao Jiang
[11]
Wei Zhang
journal
Aging
year
2020
abstract
BACKGROUND: Old age has been demonstrated to be a risk factor for GBM, but the underlying biological mechanism is still unclear. We designed this study intending to determine a mechanistic explanation for the link between age and pathogenesis in GBM. RESULTS: The expression of RPP30, an independent prognostic factor in GBM, was negatively correlated with age in both tumor and non-tumor brain samples. However, the post-transcriptional modifications carried out by RPP30 were different in primary GBM and non-tumor brain samples. RPP30 affected protein expression of cancer pathways by performing RNA modifications. Further, we found that RPP30 was related to drug metabolism pathways important in GBM. The decreased expression of RPP30 in older patients might be a pathogenic factor for GBM. CONCLUSION: This study revealed the role of RPP30 in gliomagenesis and provided the theoretical foundation for targeted therapy. METHODS: In total, 616 primary GBM samples and 41 non-tumor brain samples were enrolled in this study. Transcriptome data and clinical information were obtained from the CGGA, TCGA, and GSE53890 databases. Gene Set Variation Analysis and Gene Ontology analyses were the primary analytical methods used in this study. All statistical analyses were performed using R.
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Age-related genes were screened out by pearson correlation analysis in primary GBM (from CGGA and TCGA databases) and non-tumor brain samples (from GSE53890).
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The sequencing data of the CGGA database has been published on the CGGA portal website (http://www.cgga.org.cn/). The sequencing data of the TCGA database could be downloaded from the official website of TCGA (https://cancergenome.nih.gov). Transcriptome microarray data from non-tumor brain samples were obtained from GSE53890 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53890). All data analyzed during the study are available from the corresponding author on reasonable request.
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sections[22] "Availability of data and materials" paragraph 2
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The sequencing data of the CGGA database has been published on the CGGA portal website (http://www.cgga.org.cn/). The sequencing data of the TCGA database could be downloaded from the official website of TCGA (https://cancergenome.nih.gov). Transcriptome microarray data from non-tumor brain samples were obtained from GSE53890 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53890). All data analyzed during the study are available from the corresponding author on reasonable request.
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REST and Stress Resistance in Aging and Alzheimer’s Disease
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Complete file
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We designed this study intending to determine a mechanistic explanation for the link between age and pathogenesis in GBM.\nRESULTS: The expression of RPP30, an independent prognostic factor in GBM, was negatively correlated with age in both tumor and non-tumor brain samples. However, the post-transcriptional modifications carried out by RPP30 were different in primary GBM and non-tumor brain samples. RPP30 affected protein expression of cancer pathways by performing RNA modifications. Further, we found that RPP30 was related to drug metabolism pathways important in GBM. The decreased expression of RPP30 in older patients might be a pathogenic factor for GBM.\nCONCLUSION: This study revealed the role of RPP30 in gliomagenesis and provided the theoretical foundation for targeted therapy.\nMETHODS: In total, 616 primary GBM samples and 41 non-tumor brain samples were enrolled in this study. 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