Evidence map›Paper›PMID 39693003›Full record

ArticleGenes & genomics2025

Dual-specificity phosphatase 23 functions as a promising prognostic biomarker in non-small cell lung cancer.

Seula Keum, Yoon Ji Lee, Jung-Woong Kim, Sangmyung Rhee

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Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Seula KeumDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea.
Yoon Ji LeeDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea.
Jung-Woong KimDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea. jungkim@cau.ac.kr.
Sangmyung RheeDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea. Sangmyung.rhee@cau.ac.kr.

Funding

Ministry of Science and ICT, South Korea RS-2023-00220089Ministry of Science and ICT, South Korea RS-2024-00348828
6 · The paper itself

Abstract

backgroundThe mechanical remodeling of tumor microenvironment is critical for non-small cell lung cancer (NSCLC) progression. Dual-specificity phosphatase 23 (DUSP23) has been previously identified as a mechano-responsive gene, but its role in NSCLC progression remains unknown.

objectiveWe aim to elucidate the clinical significance of DUSP23 in NSCLC progression.

methodsWe analyzed the expression of DUSP23 in cancer using polyacrylamide hydrogels designed to mimic the stiffness of normal (soft; ~0.5 kPa) and cancerous (stiff; ~40 kPa) tissues. The prognostic significance of DUSP23 expression in patients was examined using public databases. Additionally, we conducted various cell-based assays and transcriptomic analyses in DUSP23-silenced NSCLC cell lines. A risk score prognosis model was constructed using univariate Cox regression and Kaplan-Meier analysis.

resultsOur findings show that DUSP23 is upregulated in stiff matrices and is highly associated with poor prognosis in patients with solid cancers such as NSCLC and breast cancer. Silencing of DUSP23 resulted in decreased cell proliferation and invasion. Transcriptomic profiling revealed that 182 genes were downregulated, and 230 genes upregulated following DUSP23-depletion. Notably, 182 downregulated genes were enriched in cancer-related pathways, including cell cycle progression and cytoskeleton organization. Through KEGG pathway analysis, we identified 11 cancer-related genes and developed a prognostic risk model. In this model, the high-risk group of NSCLC patients exhibited significantly shorter overall survival compared to low-risk group, based on public datasets.

conclusionOur study demonstrates the clinical significance of DUSP23 as a prognostic marker in NSCLC and highlights its potential role of DUSP23 in promoting NSCLC progression.

Indexed as

Biomarkers, TumorCarcinoma, Non-Small-Cell LungDual-Specificity PhosphatasesLung NeoplasmsMitogen-Activated Protein Kinase PhosphatasesCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMalePrognosisTumor MicroenvironmentBiomarkers, TumorDual-Specificity PhosphatasesMitogen-Activated Protein Kinase PhosphatasesBioinformatic analysisDUSP23NSCLCPrognostic biomarkerTranscriptome analysis

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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.