ArticleHuman genomics2025
Proteome-wide Mendelian randomization identifies causal plasma proteins in prostate cancer development.
Article in Human genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification ofMolecular medicine reports · 2026Article
- IL3RA identified as novel biomarker and therapeutic target for ERClinical proteomics · 2026Article
- GSTP1 as a novel protective target in sepsis: evidence from proteome-wide Mendelian randomization and multi-omics analyses.BMC infectious diseases · 2026Article
- Integrating Mendelian randomization with single-cell and spatial transcriptomics to investigate gut microbiota-associated genetic signals and molecular characteristics in prostate cancer.Frontiers in cellular and infection microbiology · 2026Article
- Evaluation of Potential Therapeutic Targets for Bacterial Infectious Skin Diseases: A Proteome-Wide Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- Proteome-wide association study of prostate cancer risk across populations.Nature communications · 2025Article
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8 authors.
Funding
Abstract
backgroundThe etiology of prostate cancer remained elusive, whether plasma protein levels are associated with prostate cancer is still unknown.
methodsWe have performed Mendelian randomization analyses to calculate the causal effects of plasma proteins on the risk of prostate cancer in the PRACTICAL consortium dataset using cis-protein quantitative trait loci (cis-pQTL) variants as instrumental variables for plasma proteins, and cis-expression quantitative trait locus (cis-eQTL) for the circulating gene expression. We also replicated the findings in the FinnGen consortium.
resultsGenetically proxied levels of 4 plasma proteins (CREB3L4, HDGF, SERPINA3, GNPNAT1) were identified as positively correlated with an increased risk of prostate cancer, while an increase in genetically proxied levels of 5 plasma proteins (TNFRSF6B, GSK3A, EIF4B, CLIC1, SMAD2) were significantly associated with a decreased risk of prostate cancer in the PRACTICAL consortium. Among the identified proteins, the causal effects of six proteins including CREB3L4, HDGF, SERPINA3, TNFRSF6B, EIF4B, and SMAD2 remained significant in the replication analyses in the FinnGen consortium and when combined with meta-analyses (SMAD2: OR 0.710, 95% CI 0.578-0.873, p-value = 0.001; CREB3L4: OR 1.260, 95% CI 1.164-1.364, p-value < 0.0001; HDGF: OR 1.072, 95% CI 1.021-1.125, p-value = 0.005; SERPINA3: OR 1.138, 95% CI 1.091-1.187, p-value < 0.0001; TNFRSF6B: OR 0.656, 95% CI 0.496-0.869, p-value = 0.003; EIF4B: OR 0.701, 95% CI 0.618-0.796, p-value < 0.0001). SMAD2 and CREB3L4 gene expressions proxied with cis-expression quantitative trait loci are also significantly associated with the risk of prostate cancer in both consortiums and when combined with meta-analyses (SMAD2: OR 0.787, 95% CI 0.719-0.861, p-value = 1.00 × 10
conclusionsOur consistent results highlighted the important roles of plasma SMAD2 and CREB3L4 in the risk of prostate cancer. Further investigations on these proteins may reveal their potential in the prevention and treatment of prostate cancer.
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