ArticleScientific reports2023
DDX52 gene expression in LUAD tissues indicates potential as a prognostic biomarker and therapeutic target.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 1 citations in OpenAlex.
- The human DDX52 protein is a nucleic acid helicase and strand annealase that promotes cell migration.Bioscience reports · 2026Article
- Unveiling the Role of SLC6A17 in Lung Adenocarcinoma: Prognosis, Pathways, and Therapeutic Implications.Current medicinal chemistry · 2026Article
- Mendelian Randomization and Bioinformatics Analysis Reveal the Potential Protective Role of Metformin in Primary Liver Cancer.Food science & nutrition · 2025Article
- Exploring the role of ELOVLs family in lung adenocarcinoma based on bioinformatic analysis and experimental validation.BMC cancer · 2025Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related morbidity and mortality globally. While DDX52, an ATP-dependent RNA helicase, plays a role in several biological processes, its specific involvement in LUAD is yet to be elucidated. We utilized ROC curves to determine DDX52's predictive potential for LUAD. Kaplan-Meier survival curves, along with univariate and multivariate Cox analyses, assessed the prognostic implications of DDX52 in LUAD. We constructed nomogram models to further delineate DDX52's influence on prognosis, employed GSEA for functional analysis, and used qRT-PCR to examine DDX52 expression in LUAD tissues. DDX52 expression was notably higher in LUAD tissues, suggesting its potential as a negative prognostic marker. We observed a direct relationship between DDX52 expression and advanced T and N stages, as well as higher grading and staging in LUAD patients. Cox analyses further underscored DDX52's role as an independent prognostic determinant for LUAD. GSEA insights indicated DDX52's influence on LUAD progression via multiple signaling pathways. Our nomogram, founded on DDX52 expression, effectively projected LUAD patient survival, as validated by calibration curves. Elevated DDX52 expression in LUAD tissues signals its potential as a poor prognostic marker. Our findings emphasize DDX52's role not only as an independent prognostic factor for LUAD but also as a significant influencer in its progression through diverse signaling pathways. The constructed nomogram also underscores the feasibility of predicting LUAD patient survival based on DDX52 expression.
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