Evidence map›Paper›PMID 31265948›Full record

ArticleMolecular therapy. Nucleic acids2019

Targeting Exosomal EBV-LMP1 Transfer and miR-203 Expression via the NF-κB Pathway: The Therapeutic Role of Aspirin in NPC.

Lielian Zuo, Yan Xie, Jinyong Tang, Shuyu Xin, Lingzhi Liu, Siwei Zhang, Qijia Yan, Fanxiu Zhu, Jianhong Lu

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

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  14. Exosomal transmission of viruses, a two-edged biological sword.Cell communication and signaling : CCS · 2023
    Review
  15. Review
  16. Article
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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

9 authors at 4 institutions in 2 countries.

Lielian ZuoNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Institute of Neuroscience, Medical College, University of South China, Hengyang 421001, Hunan, China.
Yan XieNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China.
Jinyong TangDepartment of Otolaryngology-Head and Neck Surgery, the First People's Hospital of Chenzhou, Chenzhou 423000, Hunan, China.
Shuyu XinNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China.
Lingzhi LiuNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China.
Siwei ZhangNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China.
Qijia YanNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China.
Fanxiu ZhuNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Department of Biological Science, Florida State University, Tallahassee, FL 32306, USA.
Jianhong LuNHC Key Laboratory of Carcinogenesis, Department of Pathology, Xiangya Hospital, Central South University, Changsha 410080, Hunan, China; The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Department of Microbiology, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China. Electronic address: jianhlu@csu.edu.cn.
Central South University · CNXiangya Hospital Central South University · CNChenzhou First People's Hospital · CNFlorida State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is an invasive head-and-neck tumor with Epstein-Barr virus (EBV) as an important etiological cause. The EBV oncoprotein Latent membrane protein 1 (LMP1) can be trafficked into exosomes with unclear roles, and this trafficking is a potential problem in NPC control. MicroRNA-203 (miR-203) was found by us to be downregulated by LMP1, and it functions as a tumor suppressor in NPC. In this study, aspirin reversed the epithelial-mesenchymal transition (EMT) by promoting miR-203 expression in cells, and, remarkably, it repressed exosomal LMP1 (exo-LMP1) secretion from EBV-positive cells. Nuclear factor κB (NF-κB) activation was required for the exo-LMP1 production. The exo-LMP1 uptake influenced the EMT potential of EBV-negative recipient NPC cells. The exo-LMP1 level was upregulated in clinical NPC plasma samples. Aspirin treatment observably inhibited NPC lung metastasis in nude mice. The study revealed that aspirin is a promising drug for NPC therapy via its targeting of exo-LMP1 transfer and the regulatory effect of LMP1 on miR-203 expression. EBV can regulate its own tumorigenesis via the LMP1/NF-κB/exo-LMP1 axis, opening a new avenue for understanding the pathogenesis of this tumor virus. Our study also provides a rationale for the use of exo-LMP1 or exosomal miR-203 (exo-miR203) in EBV-targeted therapy by aspirin in invasive NPC.

Indexed as

aspirinEpstein-Barr virusexosomesLatent membrane protein 1microRNA-203nasopharyngeal carcinoma

Identifiers

PMID31265948
PMCPMC6610683
OpenAlexW2949166857

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.