Evidence map›Paper›PMID 23975427›Full record

ArticleOncogene2014

NF-κB-mediated transcriptional upregulation of TNFAIP2 by the Epstein-Barr virus oncoprotein, LMP1, promotes cell motility in nasopharyngeal carcinoma.

C-C Chen, H-P Liu, M Chao, Y Liang, N-M Tsang, H-Y Huang, C-C Wu, Y-S Chang

Open access · bronzeAbstract read
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In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 86 citations in OpenAlex.

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  13. Assessing Biomarkers in Viral Infection.Advances in experimental medicine and biology · 2023
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  18. Mitochondrial transfer from mesenchymal stem cells improves neuronal metabolism after oxidant injury in vitro: The role of Miro1.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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

8 authors at 2 institutions in 1 country.

C-C ChenChang Gung Molecular Medicine Research Center, Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
H-P LiuChang Gung Molecular Medicine Research Center, Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
M ChaoGraduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
Y LiangChang Gung Molecular Medicine Research Center, Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
N-M TsangDepartments of Radiation Oncology, Chang Gung Memorial Hospital at Lin-Kou, Kwei-Shan, Taiwan.
H-Y HuangGraduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
C-C WuDepartment of Medical Biotechnology and Laboratory Science, Chang Gung University, Kwei-Shan, Taiwan.
Y-S ChangChang Gung Molecular Medicine Research Center, Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-Shan, Taiwan.
Chang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC), which is closely associated with Epstein-Barr virus (EBV), is a metastasis-prone epithelial cancer. We previously showed that tumor necrosis factor α-induced protein 2 (TNFAIP2) is highly expressed in NPC tumor tissues and is correlated with metastasis and poor survival in NPC patients. However, the underlying mechanism remains unclear. In this study, we demonstrate that the EBV oncoprotein, latent membrane protein 1 (LMP1), can transcriptionally induce TNFAIP2 expression via NF-κB. Quantitative RT-PCR and western blotting revealed that LMP1 induces TNFAIP2 expression through its C-terminal-activating region (CTAR2) domain, which is required for transduction of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling. Inhibition of NF-κB activation or depletion of p65 (a component of NF-κB) by RNA interference abolished the LMP1-induced expression of TNFAIP2, whereas ectopic expression of p65 was sufficient to induce TNFAIP2 expression. Luciferase reporter assays showed that LMP1 transcriptionally induces TNFAIP2 expression through a newly identified NF-κB-binding site within the TNFAIP2 promoter (-3,869 to -3,860 bp). Immunohistochemical analysis of NPC biopsy specimens further revealed a significant correlation between the protein levels of TNFAIP2 and activated p65 (R=0.689, P<0.001), indicating that our findings are clinically relevant. Immunofluorescence microscopy and co-immunoprecipitation assays showed that TNFAIP2 associates with actin and is involved in the formation of actin-based membrane protrusions. Furthermore, transwell migration assays demonstrated that TNFAIP2 contributes to LMP1-induced cell motility. Collectively, these findings provide novel insights into the regulation of TNFAIP2 and its role in promoting NPC tumor progression.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticTranscription, GeneticActinsCarcinomaCell Line, TumorCell Surface ExtensionsConserved SequenceCytokinesHumansNasopharyngeal CarcinomaNasopharyngeal NeoplasmsPromoter Regions, GeneticProtein Structure, TertiaryProtein TransportTranscription Factor RelAActinsCytokinesEBV-associated membrane antigen, Epstein-Barr virusTNFAIP2 protein, humanTranscription Factor RelAViral Matrix Proteins

Identifiers

PMID23975427
OpenAlexW2075562229

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.