Integrating single-cell with transcriptome-proteome Mendelian randomization reveals colorectal cancer targets
Wang S., Yao X., Li S., Wang S., Huang X., Zhou J.
Laboratory Study, published in Discov Oncol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Discov Oncol (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40381082
- PMCID
- PMC12085524
- DOI
- 10.1007/s12672-025-02636-7
- Citations
- 1
Abstract (original English)
Background Colorectal carcinogenesis involves dynamic interactions between genetic susceptibility and cellular heterogeneity, yet current studies rarely disentangle causal genes from passive associations. While GWAS have mapped numerous risk loci, only a minority colocalize with eQTL/pQTL. A multi-omics framework combining single-cell transcriptomics, transcriptomics, proteomics, and MR is urgently needed to resolve cell-type-specific drivers of colorectal cancer pathogenesis. Methods We integrated GWAS data, eQTL data, pQTL data, and single-cell RNA sequencing differential gene expression profiles from public databases. Subsequent batch Two-sample Mendelian randomization and further SMR analysis aimed to identify key genes in the pathogenesis of colorectal cancer. Results Cluster analysis identified 4909 DEGs across various cell types. We discovered that 428 DEGs had a causal association with colorectal cancer through eQTL, of which 38 genes met the FDR statistical standards, and four of these genes (CTSF, PCSK7, LYZ, LMAN2L) also had causal associations through pQTL. SMR analysis confirmed the reliability of PCSK7 as a disease target. Conclusion By integrating single-cell data, transcriptomic data, proteomic data and GWAS data for MR analysis, we identified CTSF, PCSK7, LYZ, LMAN2L as potential targets for colorectal cancer.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.