ArticleCommunications biology2024
Mendelian randomization reveals potential causal relationships between cellular senescence-related genes and multiple cancer risks.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Genome-wide association study identifies toll-like receptor four protein-mediated metabolic remodelling affecting gout pathogenesis.Journal of global health · 2026Observational
- Shengxian decoction suppresses malignant progression of lung adenocarcinoma by enhancing CD8Chinese medicine · 2026Article
- Unveiling muscle fatigue: identifying key gene biomarkers and therapeutic targets.Molecular and cellular biochemistry · 2026Article
- Macrophage polarization-related genes with potential causal roles in osteoporosis: a multi-omics Mendelian randomization study.Journal of orthopaedic surgery and research · 2026Article
- Identification of circadian rhythm-related genes in colorectal cancer by integrating bioinformatics and multi-omics mendelian randomization.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mitochondria-Related Genome-Wide Mendelian Randomization Identifies Putatively Genes for Chronic Fatigue.Molecular neurobiology · 2026Article
- Systems pharmacology approaches decipher the anti-cancer efficacy of ethnopharmacological agents in hepatocellular carcinoma.Scientific reports · 2025Article
- Bioinformatics analysis identifiesTranslational cancer research · 2025Article
- RNA-seq analysis of wild-type and mutated TBPL1 gene in breast cancer cells lines through CRISPR/Cas9 approach reveals novel molecular signatures.Scientific reports · 2025Article
- Uncovering Novel Susceptible Genes and Therapeutic Targets of Prostate Cancer: a Multi-omics Study Integrating Summary-based Mendelian Randomization Analysis and Molecular Docking.Biological procedures online · 2025Article
- Associations of plasma protein levels with risk of colorectal cancer: a proteome-wide Mendelian randomization study.Clinical proteomics · 2025Article
- Identification of cellular senescence-associated genes for predicting the diagnosis, prognosis and immunotherapy response in lung adenocarcinoma via a 113-combination machine learning framework.Discover oncology · 2025Article
- Identification of druggable targets in acute kidney injury by proteome- and transcriptome-wide Mendelian randomization and bioinformatics analysis.Biology direct · 2025Article
- Mapping fatigue: discovering brain regions and genes linked to fatigue susceptibility.Journal of translational medicine · 2025Article
- Brain imaging data and summary data-based Mendelian randomization analysis reveal the impact of multiorgan aging on schizophrenia.Frontiers in psychiatry · 2025Article
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6 authors.
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Abstract
Cellular senescence is widely acknowledged as having strong associations with cancer. However, the intricate relationships between cellular senescence-related (CSR) genes and cancer risk remain poorly explored, with insights on causality remaining elusive. In this study, Mendelian Randomization (MR) analyses were used to draw causal inferences from 866 CSR genes as exposures and summary statistics for 18 common cancers as outcomes. We focused on genetic variants affecting gene expression, DNA methylation, and protein expression quantitative trait loci (cis-eQTL, cis-mQTL, and cis-pQTL, respectively), which were strongly linked to CSR genes alterations. Variants were selected as instrumental variables (IVs) and analyzed for causality with cancer using both summary-data-based MR (SMR) and two-sample MR (TSMR) approaches. Bayesian colocalization was used to unravel potential regulatory mechanisms underpinning risk variants in cancer, and further validate the robustness of MR results. We identified five CSR genes (CNOT6, DNMT3B, MAP2K1, TBPL1, and SREBF1), 18 DNA methylation genes, and LAYN protein expression which were all causally associated with different cancer types. Beyond causality, a comprehensive analysis of gene function, pathways, and druggability values was also conducted. These findings provide a robust foundation for unravelling CSR genes molecular mechanisms and promoting clinical drug development for cancer.
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