Evidence map›Paper›PMID 41896539›Full record

ArticleCell death & disease2026

Mitofusin-2 suppresses tumor immune escape through EGFR/STAT3-mediated PD-L1 transcription.

Yan Liu, Ningning Wang, Zhenhua Li, Na Li, Fu Hui, Xinlei Wang, Gaoyan Tang, Qingyun Zhang, Guohua Yu, Shuzhen Liu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yan Liu *Oncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Ningning Wang *Oncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Zhenhua Li *Oncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Na LiOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Fu HuiOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Xinlei WangClinical College of Shandong Second Medical University, Weifang, 261000, China.
Gaoyan TangOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.ORCID http://orcid.org/0000-0001-6994-1376
Qingyun ZhangOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.
Guohua YuOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China.ORCID http://orcid.org/0009-0002-8459-416X
Shuzhen LiuOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China. liushuzhen_wf@163.com.ORCID http://orcid.org/0000-0002-8594-4486
Yanhong DingOncology Laboratory of the First Affiliated Hospital, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261000, China. rmyydingyh@sdsmu.edu.cn.ORCID http://orcid.org/0000-0002-9859-3363

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82303251
6 · The paper itself

Abstract

Immune evasion driven by aberrant PD-L1 expression poses a significant challenge to the efficacy of cancer immunotherapy. Although Mitofusin-2 (MFN2) is recognized for its role in tumor suppression, its specific contribution to the regulation of immune escape remains poorly understood. Here, we integrated analyses of public datasets, clinical specimens, and mechanistic experiments in multiple cancer cell lines, immunocompetent mouse models, and patient-derived organoids. A combination of molecular assays and single-cell transcriptomic reanalysis was employed to elucidate how MFN2 influences tumor immune escape. MFN2 expression was markedly reduced in various cancers and inversely correlated with PD-L1 levels and immunosuppressive gene signatures. Functional assays demonstrated that MFN2 suppresses PD-L1 transcription by limiting EGFR-dependent activation and nuclear translocation of STAT3. Loss of MFN2 enhanced PD-L1 expression, impaired CD8

Indexed as

B7-H1 AntigenGTP PhosphohydrolasesMitochondrial ProteinsNeoplasmsSTAT3 Transcription FactorTumor EscapeAnimalsCell Line, TumorErbB ReceptorsGene Expression Regulation, NeoplasticHumansMiceMice, Inbred C57BLSignal TransductionTranscription, GeneticB7-H1 AntigenCD274 protein, humanEGFR protein, humanErbB ReceptorsGTP PhosphohydrolasesMFN2 protein, humanMitochondrial ProteinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID41896539
PMCPMC13039860

What Socratic 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 Socratic graph.