Evidence map›Paper›PMID 35637432›Full record

ArticleBMC cancer2022

Cystatin SN promotes epithelial-mesenchymal transition and serves as a prognostic biomarker in lung adenocarcinoma.

Jian Yang, Gaomeng Luo, Chang Li, Zhunlin Zhao, Sheng Ju, Qifan Li, Zhike Chen, Cheng Ding, Xin Tong, Jun Zhao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  9. Cystatin SN (CST1) Is a Poor Independent Prognostic Biomarker for Gastrointestinal Diffuse Large B-Cell Lymphoma.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Article
  10. ZEPPI: Proteome-scale sequence-based evaluation of protein-protein interaction models.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. 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

10 authors at 2 institutions in 1 country.

Jian Yang *Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Gaomeng Luo *Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Chang Li *Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Zhunlin ZhaoDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Sheng JuDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Qifan LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Zhike ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Cheng DingDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Xin TongDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. txin@suda.edu.cn.
Jun ZhaoDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. zhaojia0327@126.com.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CN

Funding

National Natural Science Foundation of China No. 81873417
6 · The paper itself

Abstract

backgroundCystatins are a class of proteins that can inhibit cysteine protease and are widely distributed in human bodily fluids and secretions. Cystatin SN (CST1), a member of the CST superfamily, is abnormally expressed in a variety of tumors. However, its effect on the occurrence and development of lung adenocarcinoma (LUAD) remains unclear.

methodsWe obtained transcriptome analysis data of CST1 from The Cancer Genome Atlas (TCGA) and GSE31210 databases. The association of CST1 expression with prognosis, gene mutations and tumor immune microenvironment was analyzed using public databases. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were performed to investigate the potential mechanisms of CST1.

resultsIn this study, we found that CST1 was highly expressed in lung adenocarcinoma and was associated with prognosis and tumor immune microenvironment. Genetic mutations of CST1 were shown to be related to disease-free survival (DFS) by using the c-BioPortal tool. Potential proteins binding to CST1 were identified by constructing a protein-protein interaction (PPI) network. Gene set enrichment analysis (GSEA) of CST1 revealed that CST1 was notably enriched in epithelial-mesenchymal transition (EMT). Cell experiments confirmed that overexpression of CST1 promoted lung adenocarcinoma cells migration and invasion, while knockdown of CST1 significantly inhibited lung adenocarcinoma cells migration and invasion.

conclusionsOur comprehensive bioinformatics analyses revealed that CST1 may be a novel prognostic biomarker in LUAD. Experiments confirmed that CST1 promotes epithelial-mesenchymal transition in LUAD cells. These findings will help to better understand the distinct role of CST1 in LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsBiomarkersCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansPrognosisSalivary CystatinsTumor MicroenvironmentBiomarkersCST1 protein, humanSalivary CystatinsBiomarkerCystatin SN (CST1)Epithelial-mesenchymal transition (EMT)Lung adenocarcinomaTumor immune microenvironment (TIME)

Identifiers

PMID35637432
PMCPMC9150371
OpenAlexW4281625498

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LicenceCC BY
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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.