Evidence map›Paper›PMID 41258404›Full record

ArticleScientific reports2025

EVI5 unveils a role of the oncogene in modulating the Rab11/PD-L1 pathway in lung adenocarcinoma.

Tingting Cai, Yangyang Xu, Peipei Zhang, Xinyang Zhang, Jun Xie, Hui Liu, Qian He, Yongqiang Shi, Ying Qi, Qing Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. 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

12 authors.

Tingting Cai *Department of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Yangyang Xu *Department of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Peipei ZhangDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Xinyang ZhangDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Jun XieDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Hui LiuDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Qian HeDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China.
Yongqiang ShiThe First people's Hospital of Changzhou, Changzhou, China.
Ying QiThe First people's Hospital of Changzhou, Changzhou, China.
Qing LiThe First people's Hospital of Changzhou, Changzhou, China. liqblk@163.com.
Jun ZhouDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China. zhoufan@126.com.
Chong LiDepartment of Respiratory Medicine, the Third Affiliated Hospital of Soochow University, Changzhou, 213003, China. zeyou06@163.com.

Funding

Changzhou Applied Basic Research Progrem CJ20220091Changzhou Municipal Health Commission project QN202309National Natural Science Foundation of China 81970080the Science and Technology Support Plan (Social Development) Project of Changzhou CE20235057
6 · The paper itself

Abstract

Ecotropic viral integration site 5 (EVI5), a member of the Tre-2/Bub2/Cdc16 (TBC) domain-containing protein family, has been implicated in the initiation of various cancers. However, its precise role in lung adenocarcinoma (LUAD) remains unclear. This study aimed to elucidate the function of EVI5 in LUAD, with a focus on its regulation of the immune checkpoint molecule PD-L1. In the present study, we found that EVI5, Rab11 and PD-L1 were significantly overexpressed in LUAD tissues compared to adjacent normal tissues. In vitro experiments demonstrated that EVI5 knockout suppressed the expression of Rab11 and PD-L1 in LUAD cells. Notably, EVI5 overexpression promotes the expression of Rab11 and PD-L1 in LUAD cells. EVI5 was also shown to interact with Rab11 to upregulate PD-L1 expression in LUAD cells. Mechanistically, our findings identify a novel EVI5-Rab11-PD-L1 axis and suggest that EVI5 is a potential regulator of the tumor immune microenvironment, which may have implications for the efficacy of immunotherapy.

Indexed as

Adenocarcinoma of LungB7-H1 AntigenLung NeoplasmsOncogenesrab GTP-Binding ProteinsCell Cycle ProteinsCell Line, TumorGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansrab11 GTP-Binding ProteinsSignal TransductionTumor MicroenvironmentB7-H1 AntigenCD274 protein, humanCell Cycle ProteinsEVI5 protein, humanGTPase-Activating Proteinsrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsEVI5ImmunotherapyLUADPD-L1Rab11

Identifiers

PMID41258404
PMCPMC12630584

What Socratic holds

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LicenceCC BY-NC-ND
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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.