Evidence map›Paper›PMID 39958208›Full record

ArticleTranslational lung cancer research2025

Lin-Lin Fan, Xiao-Wei Wang, Xiu-Mei Zhang, Zhi-Yong Wei, Hui-Yi Wu, Qin-Xin Yang, Da Fu, Ramon Andrade de Mello, Jie-Wei Lin, Hong Yu and 1 more

Abstract read
In one paragraph

Article in Translational lung cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. [Molecular Mechanism of Neutrophils Driving the Progression of Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025
    Review
  6. Article
  7. Article
  8. Article
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.

Lin-Lin Fan *Department of Pathology, The Affiliated Taizhou People's Hospital of Dalian Medical University, Taizhou, China.
Xiao-Wei Wang *Department of Thoracic Surgery, Navy Military Medical University Affiliated Changhai Hospital, Shanghai, China.
Xiu-Mei Zhang *Department of Pathology, The People's Hospital of Xinghua City, Xinghua, China.
Zhi-Yong WeiDepartment of Pathology, Linyi People's Hospital, Linyi, China.
Hui-Yi WuDepartment of Pathology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, China.
Qin-Xin YangDepartment of Pathology, The Affiliated Taizhou People's Hospital of Dalian Medical University, Taizhou, China.
Da FuDepartment of Pathology, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, China.
Ramon Andrade de MelloDivision of Medical Oncology, Nine of July University (UNINOVE), São Paulo, SP, Brazil.
Jie-Wei LinDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Hong YuDepartment of Pathology, The Affiliated Taizhou People's Hospital of Dalian Medical University, Taizhou, China.
Geng-Xi JiangDepartment of Thoracic Surgery, Navy Military Medical University Affiliated Changhai Hospital, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Despite the recent advancements in the treatment of cancer, the 5-year survival of patients with non-small cell lung cancer (NSCLC) remains unsatisfactory. Lung adenocarcinoma (LUAD) is NSCLC's most common subtype, and metastasis is the major cause of death in patients with cancer. Therefore, identifying novel targets associated with metastasis in NSCLC is crucial to improving treatment. This study aimed to characterize the expression of GNGT1 in LUAD and to clarify the mechanism underlying the association between the higher expression level of GNGT1 and worse prognosis in patients. Methods: The transcriptome datasets and clinical information of patients with LUAD were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Bioinformatics analyses were performed in 515 patients who were stratified into two groups (high- and low-GNGT1 expression group) according to the GNGT1 level. Overall survival, DNA promotor methylation, immune cell infiltration, gene set enrichment analysis (GSEA), and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to elucidate the functions of GNGT1 and to identify the related hub genes in LUAD. Their expression and functions in LUAD were verified using tissues from patients and transgenic mice overexpressing GNGT1 under the control of a lung-specific promoter (Scgb1a1-Cre). Results: GNGT1 was overexpressed in patients with LUAD and was associated with poor prognosis. GNGT1 expression was significantly correlated with gene alteration and hypomethylated promoter status. High GNGT1 expression in patients with LUAD was associated with advanced lymph node metastasis and the degree of immune cell infiltration. Functional enrichment analyses indicated that differentially expressed genes (DEGs) in the high-GNGT1 group participated in DNA replication, DNA replication preinitiation, and M phase, while cell adhesion molecules, apoptosis, and natural killer cell-mediated cytotoxicity were all downregulated. Messenger RNA and protein levels were correspondingly regulated in human LUAD tissues and the Scgb1a1-Cre; LSL-GNGT1 mouse model (GNGT1 Conclusions: GNGT1 was associated with tumor cell proliferation via the enhancement of tumor cell stemness and interaction with driver genes. Elevated GNGT1 expression promoted epithelial-mesenchymal transformation, remodeled the tumor microenvironment, and led to tumor metastasis, ultimately worsening the survival-related prognosis of patients with LUAD.

Indexed as

GNGT1neutrophils extracellular traps (NETs)stemnesstumor microenvironment (TME)

Identifiers

PMID39958208
PMCPMC11826275

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.