Evidence map›Paper›PMID 35672776›Full record

ArticleJournal of translational medicine2022

Junctional adhesion molecule-like protein promotes tumor progression via the Wnt/β-catenin signaling pathway in lung adenocarcinoma.

Qian Wu, Rui Li, Qing-Xiang Wang, Meng-Yu Zhang, Ting-Ting Liu, Yi-Qing Qu

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% of its field
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

12 citing papers in PubMed, 16 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Qian WuDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China.
Rui LiDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China.
Qing-Xiang WangDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China.
Meng-Yu ZhangDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China.
Ting-Ting LiuDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China.
Yi-Qing QuDepartment of Pulmonary and Critical Care Medicine, Shandong Key Laboratory of Infectious Respiratory Diseases, Qilu Hospital of Shandong University, Jinan, 250012, China. quyiqing@sdu.edu.cn.ORCID 0000-0002-9538-7601
Qilu Hospital of Shandong University · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is a heavy social burden worldwide. Because the mechanisms involved in LUAD remain unclear, the prognosis of LUAD remains poor. Consequently, it is urgent to investigate the potential mechanisms of LUAD. Junctional adhesion molecule-like protein (JAML), is recognized as a tumorigenesis molecule in gastric cancer. However, the role of JAML in LUAD is still unclear. Here we aimed to evaluate the role of JAML in LUAD.

methodsqRT-PCR, Western blotting and immunohistochemistry were conducted to investigate the expression of JAML in LUAD tissues. JAML was knocked down and overexpressed in LUAD cells using transient transfection by siRNA and plasmids or stable transfection by lentivirus. Proliferation potential of LUAD cells were detected by Cell Counting Kit-8, EdU incorporation and Colony formation assay. Migration and invasion abilities of LUAD cells were determined by wound healing, transwell migration and invasion assays. Cell cycle and cell apoptosis were detected by flow cytometry. The effects of JAML in vivo were studied in xenograft tumor models. Western blotting was used to explore the molecular mechanisms of JAML function. In addition, rescue experiments were performed to verify the possible mechanisms.

resultsJAML expression was elevated in LUAD tissues compared with peritumor tissues, and this upregulation was positively related to pT and pTNM. Furthermore, both in vitro and in vivo, JAML silencing markedly repressed malignant behaviors of LUAD cells and vice versa. Knockdown of JAML also mediated cell cycle arrest at G

conclusionsOur data reveal the oncogenic role of JAML in LUAD, indicating that JAML may be a predictive biomarker and novel therapeutic target for LUAD.

Indexed as

AdenocarcinomaAdenocarcinoma of LungLung Neoplasmsbeta CateninCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansJunctional Adhesion MoleculesWnt Signaling Pathwaybeta CateninCell Adhesion MoleculesJAML protein, humanJunctional Adhesion MoleculesInvasionJunctional adhesion molecule-like proteinLung adenocarcinomaMigrationTumor progression

Identifiers

PMID35672776
PMCPMC9171988
OpenAlexW4281762949

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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.