Evidence map›Paper›PMID 32668393›Full record

ArticleMolecular therapy. Nucleic acids2020

Dissecting the Functional Mechanisms of Somatic Copy-Number Alterations Based on Dysregulated ceRNA Networks across Cancers.

Yanyan Ping, Yao Zhou, Jing Hu, Lin Pang, Chaohan Xu, Yun Xiao

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 18 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

6 authors at 1 institution in 1 country.

Yanyan PingCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China.
Yao ZhouCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China.
Jing HuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China.
Lin PangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China.
Chaohan XuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China. Electronic address: chaohanxu@hrbmu.edu.cn.
Yun XiaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China; Key Laboratory of Cardiovascular Medicine Research, Harbin Medical University, Harbin, Heilongjiang 150086, China. Electronic address: xiaoyun@ems.hrbmu.edu.cn.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic copy-number alterations (SCNAs) drive tumor growth and evolution. However, the functional roles of SCNAs across the genome are still poorly understood. We provide an integrative strategy to characterize the functional roles of driver SCNAs in cancers based on dysregulated competing endogenous RNA (ceRNA) networks. We identified 44 driver SCNAs in lower-grade glioma (LGG). The dysregulated patterns losing all correlation relationships dominated dysregulated ceRNA networks. Homozygous deletion of six genes in 9p21.3 characterized an LGG subtype with poor prognosis and contributed to the dysfunction of cancer-associated pathways in a complementary way. The pan-cancer analysis showed that different cancer types harbored different driver SCNAs through dysregulating the crosstalk with common ceRNAs. The same SCNAs destroyed their ceRNA networks through different miRNA-mediated ceRNA regulations in different cancers. Additionally, some SCNAs performed different functional mechanisms in different cancers, which added another layer of complexity to cancer heterogeneity. Compared with previous methods, our strategy could directly dissect functional roles of SCNAs from the view of ceRNA networks, which not only complemented the functions of protein-coding genes but also provided a new avenue to characterize the functions of noncoding RNAs. Also, our strategy could be applied to more types of cancers to identify pathogenic mechanism driven by the SCNAs.

Identifiers

PMID32668393
PMCPMC7358224
OpenAlexW3036157869

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.