Evidence map›Paper›PMID 31731581›Full record

ArticleCancers2019

Emodin Inhibits EBV Reactivation and Represses NPC Tumorigenesis.

Chung-Chun Wu, Mei-Shu Chen, Yu-Jhen Cheng, Ying-Chieh Ko, Su-Fang Lin, Ing-Ming Chiu, Jen-Yang Chen

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-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

20 citing papers in PubMed, 26 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

7 authors at 1 institution in 1 country.

Chung-Chun WuNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town 350, Taiwan.
Mei-Shu ChenInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan Town 350, Taiwan.
Yu-Jhen ChengNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town 350, Taiwan.
Ying-Chieh KoNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town 350, Taiwan.
Su-Fang LinNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town 350, Taiwan.ORCID 0000-0001-8706-2439
Ing-Ming ChiuInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan Town 350, Taiwan.ORCID 0000-0001-6512-9815
Jen-Yang ChenNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town 350, Taiwan.
National Health Research Institutes · TW

Funding

ministry of science and technology 108-2320-B-400 -019
6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a unique malignancy derived from the epithelium of the nasopharynx. Despite great advances in the development of radiotherapy and chemotherapy, relapse and metastasis in NPC patients remain major causes of mortality. Evidence accumulated over recent years indicates that Epstein-Barr virus (EBV) lytic replication plays an important role in the pathogenesis of NPC and inhibition of EBV reactivation is now being considered as a goal for the therapy of EBV-associated cancers. With this in mind, a panel of dietary compounds was screened and emodin was found to have potential anti-EBV activity. Through Western blotting, immunofluorescence, and flow cytometric analysis, we show that emodin inhibits the expression of EBV lytic proteins and blocks virion production in EBV- positive epithelial cell lines. In investigating the underlying mechanism, reporter assays indicated that emodin represses Zta promoter (Zp) and Rta promoter (Rp) activities, triggered by various inducers. Mapping of the Zp construct reveals that the SP1 binding region is important for emodin-triggered repression and emodin is shown to be able to inhibit SP1 expression, suggesting that it likely inhibits EBV reactivation by suppression of SP1 expression. Moreover, we also show that emodin inhibits the tumorigenic properties induced by repeated EBV reactivation, including micronucleus formation, cell proliferation, migration, and matrigel invasiveness. Emodin administration also represses the tumor growth in mice which is induced by EBV activation. Taken together, our results provide a potential chemopreventive agent in restricting EBV reactivation and NPC recurrence.

Indexed as

emodinEpstein-Barr virusnasopharyngeal carcinomareactivationrelapse

Identifiers

PMID31731581
PMCPMC6896023
OpenAlexW2985046425

What OpenQuestion 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 OpenQuestion graph.