Evidence map›Paper›PMID 42141449›Full record

ArticleCell communication and signaling : CCS2026

EBV (LMP1) enhances cisplatin resistance by enhancing degradation of interferon regulatory factor 3.

Yueshuo Li, Na Liu, Chenxing Yang, Shan He, Cheng Luo, Lin Wang, Min Tang, Xiangjian Luo, Ya Cao, Li Shang and 1 more

Abstract read
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In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Yueshuo LiDepartment of Pathology, National Clinical Research Center for Geriatric Diseases (Xiangya Hospital), Central South University, Changsha, 410078, China.
Na LiuKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Chenxing YangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Shan HeKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Cheng LuoDepartment of Pathology, National Clinical Research Center for Geriatric Diseases (Xiangya Hospital), Central South University, Changsha, 410078, China.
Lin WangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Min TangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Xiangjian LuoKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Ya CaoKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, 410078, China.
Li ShangDepartment of Pathology, National Clinical Research Center for Geriatric Diseases (Xiangya Hospital), Central South University, Changsha, 410078, China. Shangli1212@csu.edu.cn.
Feng ShiDepartment of Pathology, National Clinical Research Center for Geriatric Diseases (Xiangya Hospital), Central South University, Changsha, 410078, China. Shi_feng@csu.edu.cn.

Funding

Hunan Provincial Natural Science Foundation of China 2022JJ20083Hunan Provincial Natural Science Foundation of China 2025JJ60499National Natural Science Foundation of China 82303137National Natural Science Foundation of China 82573064, 82073030
6 · The paper itself

Abstract

EBV employs multiple strategies to subvert host innate immunity, including suppression of type I IFN signaling. However, the precise mechanism by which its latent oncoprotein LMP1 modulates this pathway in nasopharyngeal carcinoma (NPC) remains unclear. Here, we demonstrated that LMP1 enhances the interaction between interferon regulatory factor 3 (IRF3) and E3 ubiquitin ligase Ro52, which leads to the degradation of IRF3 protein. Low IRF3 expression correlates with poor prognosis in NPC patients. Notably, IRF3 may inhibit cell G1/S transition by directly inducing CDKN2C transcription, which suggests the direct effect as a moonlighting protein in regulating cell cycle. Cisplatin is an effective DNA-damaging anti-tumor agent which may activate type I IFNs-mediated anti-tumor immunity by stimulating the release of dsDNA. EBV (LMP1) inhibits cisplatin-activated type I IFN signaling by reducing IRF3 expression. The activation of IRF3 enhances the sensitivity of EBV (LMP1)-positive NPC cells to cisplatin in vitro and in vivo. These findings establish the LMP1-Ro52-IRF3 axis as a critical immune evasion mechanism that drives cisplatin resistance and suggest that targeting this axis represents a viable strategy to enhance chemotherapy efficacy in EBV-positive NPC.

Indexed as

CisplatinDrug Resistance, NeoplasmHerpesvirus 4, HumanInterferon Regulatory Factor-3ProteolysisViral Matrix ProteinsAnimalsAntineoplastic AgentsCell Line, TumorHumansNasopharyngeal CarcinomaSignal TransductionUbiquitin-Protein LigasesAntineoplastic AgentsCisplatinEBV-associated membrane antigen, Epstein-Barr virusInterferon Regulatory Factor-3IRF3 protein, humanUbiquitin-Protein LigasesViral Matrix ProteinsCisplatin resistanceEpstein-Barr virusInterferon regulatory factor 3Nasopharyngeal carcinomaUbiquitination

Identifiers

PMID42141449
PMCPMC13343618

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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.