ArticleInternational urology and nephrology2025
Identification of druggable genetic targets for prostate cancer risk based on mendelian randomization and single-cell RNA sequencing.
Article in International urology and nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mitochondria-Related Genome-Wide Mendelian Randomization Identifies Putatively Genes for Chronic Fatigue.Molecular neurobiology · 2026Article
- Mendelian randomization analysis of druggable gene expression in liver cancer risk and autoimmune hepatitis.Discover oncology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
purposeThis study aimed to identify genetic targets linked to prostate cancer risk using advanced genetic analysis techniques.
objectiveThe goal was to conduct a comprehensive analysis using Mendelian Randomization (MR), colocalization, and single-cell RNA sequencing to identify druggable genes as potential therapeutic targets or diagnostic markers.
methodsThe study involved selecting 2608 druggable genes by intersecting expression Quantitative Trait Loci (eQTLs) with druggable genome databases. MR analysis using prostate cancer GWAS data identified genes with causal associations to prostate cancer risk. Colocalization analysis confirmed shared genetic variants influencing both the exposure and outcome. Single-cell RNA sequencing assessed gene expression in prostate tumor cell types, while a phenome-wide association study (PheWAS) evaluated potential side effects.
resultsMR analysis identified 58 genes associated with prostate cancer risk, with 12 validated by colocalization analysis. Five genes (BAK1, ATP1B2, PEMT, TPM3, ZDHHC7) demonstrated strong colocalization, indicating potential as drug targets. Single-cell RNA sequencing revealed their enrichment in prostate tumor T cells and macrophages. PheWAS suggested minimal side effects for most, except BAK1, which was linked to increased platelet counts.
conclusionThis study identified several genetic targets associated with prostate cancer risk, highlighting the potential for targeted therapy. By integrating Mendelian randomization analysis, colocalization analysis, and single-cell RNA sequencing, the accuracy of target validation was improved, which may provide new directions for targeted therapy in prostate cancer.
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