Evidence map›Paper›PMID 33795637›Full record

ArticleCell death & disease2021

EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma.

San Xu, Zhuan Zhou, Xingzhi Peng, Xuxiu Tao, Peijun Zhou, Kun Zhang, Jinwu Peng, Dan Li, Liangfang Shen, Lifang Yang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

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  10. Inflammasomes and autophagy in cancer: unlocking targeted therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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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

10 authors at 2 institutions in 3 countries.

San Xu *Department of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Zhuan Zhou *Department of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Xingzhi PengDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Xuxiu TaoDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Peijun ZhouDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Kun ZhangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Jinwu PengDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, China.
Dan LiInstitute of Molecular Medicine and Oncology, College of Biology, Hunan University, Changsha, China.
Liangfang ShenDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Lifang YangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China. yanglifang@csu.edu.cn.ORCID 0000-0002-3012-8350
Central South University · CNHunan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have indicated that dysfunction of autophagy is involved in the initiation and progression of multiple tumors and their chemoradiotherapy. Epstein-Barr virus (EBV) is a lymphotropic human gamma herpes virus that has been implicated in the pathogenesis of nasopharyngeal carcinoma (NPC). EBV encoded latent membrane protein1 (LMP1) exhibits the properties of a classical oncoprotein. In previous studies, we experimentally demonstrated that LMP1 could increase the radioresistance of NPC. However, how LMP1 contributes to the radioresistance in NPC is still not clear. In the present study, we found that LMP1 could enhance autophagy by upregulating the expression of BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3). Knockdown of BNIP3 could increase the apoptosis and decrease the radioresistance mediated by protective autophagy in LMP1-positive NPC cells. The data showed that increased BNIP3 expression is mediated by LMP1 through the ERK/HIF1α signaling axis, and LMP1 promotes the binding of BNIP3 to Beclin1 and competitively reduces the binding of Bcl-2 to Beclin1, thus upregulating autophagy. Furthermore, knockdown of BNIP3 can reduce the radioresistance promoted by protective autophagy in vivo. These data clearly indicated that, through BNIP3, LMP1 induced autophagy, which has a crucial role in the protection of LMP1-positive NPC cells against irradiation. It provides a new basis and potential target for elucidating LMP1-mediated radioresistance.

Indexed as

ApoptosisAutophagyCell Line, TumorEpstein-Barr Virus InfectionsGene Expression Regulation, NeoplasticHerpesvirus 4, HumanHumansMembrane ProteinsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsProto-Oncogene ProteinsViral Matrix ProteinsBNIP3 protein, humanEBV-associated membrane antigen, Epstein-Barr virusMembrane ProteinsProto-Oncogene ProteinsViral Matrix Proteins

Identifiers

PMID33795637
PMCPMC8016912
OpenAlexW3139878747

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.