Evidence map›Paper›PMID 31719831›Full record

ArticleFrontiers in genetics2019

Identification of Dysregulated Competitive Endogenous RNA Networks Driven by Copy Number Variations in Malignant Gliomas.

Jinyuan Xu, Xiaobo Hou, Lin Pang, Shangqin Sun, Shengyuan He, Yiran Yang, Kun Liu, Linfu Xu, Wenkang Yin, Chaohan Xu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Jinyuan XuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Xiaobo HouCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Lin PangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Shangqin SunCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Shengyuan HeCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Yiran YangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Kun LiuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Linfu XuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Wenkang YinCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Chaohan XuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Yun XiaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas represent 80% of malignant brain tumors. Because of the high heterogeneity, the oncogenic mechanisms in gliomas are still unclear. In this study, we developed a new approach to identify dysregulated competitive endogenous RNA (ceRNA) interactions driven by copy number variation (CNV) in both lower-grade glioma (LGG) and glioblastoma multiforme (GBM). By analyzing genome and transcriptome data from The Cancer Genome Atlas (TCGA), we first found out the protein coding genes and long non-coding RNAs (lncRNAs) significantly affected by CNVs and further determined CNV-driven dysregulated ceRNA interactions by a customized pipeline. We obtained 13,776 CNV-driven dysregulated ceRNA pairs (including 3,954 mRNAs and 306 lncRNAs) in LGG and 262 pairs (including 221 mRNAs and 11 lncRNAs) in GBM, respectively. Our results showed that most of the ceRNA interactions were weakened by CNVs in both LGG and GBM, and many CNV-driven genes shared the same ceRNAs in the dysregulated ceRNA networks. Functional analysis indicated that the CNV-driven ceRNA network involved in some important mechanisms of tumorigenesis, such as cell cycle, p53 signaling pathway and TGF-beta signaling pathway. Further investigation of the ceRNA pairs in the communities from the dysregulated ceRNA network revealed more detailed biological functions related to the oncogenesis of malignant gliomas. Moreover, by exploring the association of CNV-driven ceRNAs with prognosis and histological subtype, we found that the copy number status of MTAP, KLHL9, and ELAVL2 related to the overall survival in LGG and showed high correlation with histological subtype. In conclusion, this study provided new insight into the molecular mechanisms and clinical biomarkers in gliomas.

Indexed as

ceRNACNVgliomaslncRNAprognosis

Identifiers

PMID31719831
PMCPMC6827427
OpenAlexW2982695563

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.