Evidence map›Paper›PMID 41430237›Full record

ArticleJournal of translational medicine2025

CD155 reprograms glycolysis via the YAP/TEAD1-GLUT1 axis to promote lung adenocarcinoma progression and M2 macrophage polarization: a metabolic-immune target visualized by

Zhiming Cheng, Shu Wang, Shuoyan Xu, Yuxiang Wang, Yao Diao, Bulin Du, Xuena Li, Yaming Li

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Article in Journal of translational medicine, 2025. 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

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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. Review
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

8 authors.

Zhiming Cheng *Department of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Shu Wang *Department of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Shuoyan XuDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Yuxiang WangDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Yao DiaoDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Bulin DuDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Xuena LiDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China.
Yaming LiDepartment of Nuclear Medicine, The First Hospital of China Medical University, No. 155, Nanjing Northern Street, Shenyang, 110001, Liaoning, People's Republic of China. ymli2001@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD155, an emerging immune checkpoint, contributes to tumor immune evasion and progression, but its roles in metabolic reprogramming and tumor-associated macrophages (TAMs) polarization in lung adenocarcinoma (LUAD) remain uncharacterized. This study combines molecular biology, metabolic imaging, and clinical data to elucidate CD155's dual role in driving LUAD progression through glycolytic rewiring and immunosuppressive TAMs polarization.

methodsThrough immunohistochemistry (IHC) and

resultsCD155 was significantly overexpressed in LUAD tissues and positively correlated with advanced TNM stage, lymph node metastasis and elevated

conclusionsWe identify a novel CD155/YAP/TEAD1/GLUT1 axis that reprograms LUAD metabolism and facilitates immunosuppressive tumor microenvironment formation. CD155 functions as a metabolic-immune hub in LUAD, and its targeting could simultaneously suppress tumor growth and restore antitumor immunity, offering dual therapeutic advantages. Clinically,

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinoma of LungDisease ProgressionDNA-Binding ProteinsFluorodeoxyglucose F18Glucose Transporter Type 1GlycolysisLung NeoplasmsMacrophagesPositron Emission Tomography Computed TomographyTranscription FactorsAnimalsCell Line, TumorFemaleHumansMaleAdaptor Proteins, Signal TransducingDNA-Binding ProteinsFluorodeoxyglucose F18Glucose Transporter Type 1poliovirus receptorReceptors, VirusSLC2A1 protein, humanTEAD1 protein, humanTEA Domain Transcription FactorsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsCD155GlycolysisLung adenocarcinomaMacrophage polarizationTEAD1YAP

Identifiers

PMID41430237
PMCPMC12903674

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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.