Evidence map›Paper›PMID 39838844›Full record

ArticleCancer reports (Hoboken, N.J.)2025

Aberrant Expression of JAM2 Inhibits Invasion and Migration in Lung Adenocarcinoma.

Jun Chen, Yuan Cui, Zhimeng Chen, Hao Ding, Chang Li, Sheng Ju, Cheng Ding, Chun Xu, Jun Zhao, Xin Tong

Abstract read
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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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.

Jun ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Yuan CuiDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0001-8199-6599
Zhimeng ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0009-0003-7841-9207
Hao DingDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Chang LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Sheng JuDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Cheng DingDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Chun XuDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jun ZhaoDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xin TongDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.

Funding

First Affiliated Hospital of Soochow University BXQN202133Natural Science Foundation of Jiangsu Province BK20220250
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer. JAM2, a member of the Junctional adhesion molecule (JAM) family, plays diverse roles in cell-cell contacts and tumor development. Although JAM2's expression and functions have been reported in various cancers, its clinical and biological significance in LUAD remains unclear.

aimsThe aim of this study was to investigate the expression and function of JAM2 in LUAD, and to assess its potential as a prognostic gene and a molecular target for early diagnosis and targeted therapy. MATERIALS: Immunohistochemistry (IHC) was performed on 37 pairs of LUAD tissues. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted among co-expression genes in different JAM2 subgroups. In vitro experiments were also conducted to study the migratory and invasive capabilities of LUAD cells when JAM2 was overexpressed.

resultsThe study confirmed that JAM2 was downregulated in LUAD, possibly due to methylation. JAM2 emerged as an independent prognostic gene for predicting the outcomes of patients with LUAD. IHC analysis revealed the significance of JAM2 with clinicopathological parameters in LUAD. GO and KEGG analyses provided insights into the biological processes and pathways associated with JAM2. In vitro experiments showed that overexpressing JAM2 significantly suppressed the migratory and invasive capabilities of LUAD cells. Additionally, JAM2 played a crucial role in LUAD inflammatory infiltration, and higher JAM2 expression predicted a better immunotherapy response.

conclusionJAM2 may serve as a promising molecular target for early diagnosis and targeted therapy of LUAD. Its downregulation in LUAD, potential role as a prognostic gene, and influence on cell migration, invasion, and inflammatory infiltration make it a valuable target for further research and development of therapeutic strategies.

Indexed as

Adenocarcinoma of LungBiomarkers, TumorCell Adhesion MoleculesLung NeoplasmsAgedCell Line, TumorCell MovementDNA MethylationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm InvasivenessPrognosisBiomarkers, TumorCell Adhesion Moleculeshypermethylationimmune cells infiltrationinvasionJAM2lung adenocarcinomamigration

Identifiers

PMID39838844
PMCPMC11751475

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