Evidence map›Paper›PMID 41454420›Full record

ArticleHereditas2025

Integrated transcriptomic and functional analysis reveals overlapping pathways in lung adenocarcinoma and chronic obstructive pulmonary disease.

Dan Zhu, Jun Zhu

Abstract read
In one paragraph

Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Dan ZhuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Shaoyang University, Shaoyang, 422000, China.
Jun ZhuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Shaoyang University, Shaoyang, 422000, China. zhujun3455@outlook.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality, with chronic obstructive pulmonary disease (COPD) identified as a major risk factor. However, the molecular overlap between LUAD and COPD remains poorly understood. This study aimed to identify shared hub genes and to evaluate their functional significance in LUAD.

methodsDifferential gene expression analysis was conducted using two LUAD (GSE19188, GSE18842, and GSE31210) and two COPD (GSE76925, GSE57148, and GSE137557) datasets from the Gene Expression Omnibus (GEO) database. Common hub genes were identified by Venn diagram intersection of the top 3,000 DEGs per dataset. Validation was performed via RT-qPCR in LUAD (A549 and H1299) and COPD cell models. Additional transcriptomic and proteomic validations were done using GSCA, OncoDB, and HPA databases. miRNA–mRNA interactions were predicted using TargetScan and validated by TaqMan RT-qPCR. Functional assays, including CCK-8, colony formation, and wound healing, were performed after overexpression of SYNE1 and SULT1A1 in LUAD cell lines.

resultsFour common hub genes, including SYNE1, SULT1A1, FAM76A, and COL10A1 were identified in both LUAD and COPD. SYNE1, SULT1A1, and FAM76A were significantly downregulated, while COL10A1 was upregulated. miRNAs targeting these genes (miR-22-3p, miR-17-3p, miR-455-3p.2, and miR-1297) were significantly upregulated in LUAD and COPD models. Immune correlation analysis revealed associations between hub gene expression and immune subtypes, immune checkpoint regulators, and drug resistance. Functional assays demonstrated that overexpression of SYNE1 and SULT1A1 suppressed proliferation, colony formation, and migration in LUAD cells. Immune correlation analysis revealed associations between hub gene expression and immune subtypes, immune checkpoint regulators, and drug resistance.

conclusionThis study identifies shared molecular signatures between LUAD and COPD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsPulmonary Disease, Chronic ObstructiveTranscriptomeCell Line, TumorGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMicroRNAsMicroRNAsBiomarkerCOPDHub genesLUADTreatment

Identifiers

PMID41454420
PMCPMC12849426

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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.