Evidence map›Paper›PMID 26517512›Full record

ArticleOncotarget2015

The copy number of Epstein-Barr virus latent genome correlates with the oncogenicity by the activation level of LMP1 and NF-κB.

Lielian Zuo, Haibo Yu, Lingzhi Liu, Yunlian Tang, Hongzhuan Wu, Jing Yang, Meijuan Zhu, Shujuan Du, Lian Zhao, Li Cao and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 33 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

12 authors at 6 institutions in 2 countries.

Lielian ZuoCentral Laboratory, Hunan Provincial Tumor Hospital, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, China.
Haibo YuCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Lingzhi LiuCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Yunlian TangCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Hongzhuan WuDepartment of Biological Sciences, Alabama State University, Montgomery, AL 36101, USA.
Jing YangCentral Laboratory, Hunan Provincial Tumor Hospital, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, China.
Meijuan ZhuCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Shujuan DuCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Lian ZhaoCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Li CaoCancer Research Institute, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, School of Basic Medical Science, Central South University, Changsha, Hunan 410078, China.
Guiyuan LiCentral Laboratory, Hunan Provincial Tumor Hospital, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, China.
Jianhong LuCentral Laboratory, Hunan Provincial Tumor Hospital, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, China.
Central South University · CNHunan Cancer Hospital · CNAlabama State University · USSecond Xiangya Hospital of Central South University · CNThird Xiangya Hospital · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A tumor model that Epstein-Barr virus (EBV) latent infection facilitated the tumorigenicity was previously established using the Maxi-EBV system. In the present approach, EBV-lost cell clones demonstrated significantly decreased tumorigenesis. On the other hand, the LMP1 gene in Maxi-EBV genome was replaced by that of nasopharyngeal carcinoma origin. The resultant cell line, 293-1/NL showed much lower malignancy than the original 293-EBV. The result was opposite to our expectation. The change of 293 sublineage cells for EBV harboring also got similar result. To seek the underlying reason, the copy number of EBV genome in all the cell lines was detected. The result indicated that 293-EBV contained about 4.5-fold higher EBV copies than 293-1/NL did. Parallel EBV genomes led to relatively stable copies in different 293 sublineages, suggesting the viral genome structure is a factor for the sustainability of EBV's copy number. Moreover, the LMP1 transcription in high copy-containing cells showed abnormally high level. Furthermore, the main LMP1-driven pathway, transcription factor NF-κB, was highly activated in high-copy cells. Here we first manifest by experimental model that the copy number of EBV latent genome correlates with the viral pathogenesis, which depends on the activation level of LMP1 and NF-κB. Overall, both the presence and amount of EBV genome are crucial for the viral oncogenicity.

Indexed as

AnimalsBlotting, WesternCell Transformation, NeoplasticGene DosageGene Expression Regulation, ViralGenome, ViralHEK293 CellsHerpesvirus 4, HumanHost-Pathogen InteractionsHumansMice, Inbred BALB CMice, NudeNeoplasms, ExperimentalNF-kappa BReverse Transcriptase Polymerase Chain ReactionSignal TransductionEBV-associated membrane antigen, Epstein-Barr virusNF-kappa BViral Matrix Proteinscopy numberEpstein-Barr viruslatent genomelatent membrane protein 1oncogenicity

Identifiers

PMID26517512
PMCPMC4747387
OpenAlexW1840159192

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.