ArticleAmerican journal of human genetics2021
H3K27ac HiChIP in prostate cell lines identifies risk genes for prostate cancer susceptibility.
Article in American journal of human genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 51 citations in OpenAlex.
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- Causal relationships between alzheimer's disease genetics and brain connectivity alterations: a multi-modal mendelian randomization study with transcriptomic validation of 191 rs-fMRI and 635 DTI neuroimaging traits.Brain imaging and behavior · 2026Article
- Regulation of androgen receptor expression by enhancer elements in prostate cancer.Experimental & molecular medicine · 2026Review
- Integrative genomic profiling identifies MLPH as a candidate gene in prostate cancer.Frontiers in medicine · 2026Article
- Non-coding genetic variants underlying higher prostate cancer risk in men of African ancestry.Nature communications · 2025Article
- Exploring the Impact of Nanotherapeutics on Histone H3 and H4 Acetylation Enrichment in Cancer Epigenome: A Systematic Scoping Synthesis.Epigenomes · 2025Review
- Wnt signaling activation induces CTCF binding and loop formation atGenome research · 2025Article
- Loop Catalog: a comprehensive HiChIP database of human and mouse samples.Genome biology · 2025Article
- Chrombus-XMBD: a graph convolution model predicting 3D-genome from chromatin features.Briefings in bioinformatics · 2025Article
- CRISPR screening identifies regulators of enhancer-mediated androgen receptor transcription in advanced prostate cancer.Cell reports · 2025Article
- Biological determinants of PSMA expression, regulation and heterogeneity in prostate cancer.Nature reviews. Urology · 2025Review
- Decoding the epigenetics and chromatin loop dynamics of androgen receptor-mediated transcription.Nature communications · 2024Article
- Targeting mRNA-coding genes in prostate cancer using CRISPR/Cas9 technology with a special focus on androgen receptor signaling.Cell communication and signaling : CCS · 2024Review
- Identifying genetic variants associated with chromatin looping and genome function.Nature communications · 2024Article
- Genomic and transcriptomic features of androgen receptor signaling inhibitor resistance in metastatic castration-resistant prostate cancer.The Journal of clinical investigation · 2024Article
- HiChIP-Based Epigenomic Footprinting Identifies a Promoter Variant of UXS1 That Confers Genetic Susceptibility to Gastroesophageal Cancer.Cancer research · 2024Article
- Integrative high-throughput enhancer surveying and functional verification divulges a YY2-condensed regulatory axis conferring risk for osteoporosis.Cell genomics · 2024Article
- A Bayesian fine-mapping model using a continuous global-local shrinkage prior with applications in prostate cancer analysis.American journal of human genetics · 2024Article
- The PENGUIN approach to reconstruct protein interactions at enhancer-promoter regions and its application to prostate cancer.Nature communications · 2023Article
- Compartmentalization of androgen receptors at endogenous genes in living cells.Nucleic acids research · 2023Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Genome-wide association studies (GWASs) have identified more than 200 prostate cancer (PrCa) risk regions, which provide potential insights into causal mechanisms. Multiple lines of evidence show that a significant proportion of PrCa risk can be explained by germline causal variants that dysregulate nearby target genes in prostate-relevant tissues, thus altering disease risk. The traditional approach to explore this hypothesis has been correlating GWAS variants with steady-state transcript levels, referred to as expression quantitative trait loci (eQTLs). In this work, we assess the utility of chromosome conformation capture (3C) coupled with immunoprecipitation (HiChIP) to identify target genes for PrCa GWAS risk loci. We find that interactome data confirm previously reported PrCa target genes identified through GWAS/eQTL overlap (e.g., MLPH). Interestingly, HiChIP identifies links between PrCa GWAS variants and genes well-known to play a role in prostate cancer biology (e.g., AR) that are not detected by eQTL-based methods. HiChIP predicted enhancer elements at the AR and NKX3-1 prostate cancer risk loci, and both were experimentally confirmed to regulate expression of the corresponding genes through CRISPR interference (CRISPRi) perturbation in LNCaP cells. Our results demonstrate that looping data harbor additional information beyond eQTLs and expand the number of PrCa GWAS loci that can be linked to candidate susceptibility genes.
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