ArticleGenome biology2018
CRISPR-mediated deletion of prostate cancer risk-associated CTCF loop anchors identifies repressive chromatin loops.
Article in Genome biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.Non-coding RNA research · 2026Review
- Decoding 3D chromatin architecture reveals distinct enhancer classes underlying hierarchical gene regulation in prostate cancer.Genome biology · 2026Article
- Engineering the Link: From Genome Interaction Maps to Functional Insight.Advanced biology · 2025Review
- Ectopic Recruitment of the CTCF N-Terminal Domain with Two Proximal Zinc-Finger Domains as a Tool for 3D Genome Engineering.International journal of molecular sciences · 2025Article
- Methyl-Micro-C: simultaneous characterization of chromatin accessibility, interactions, and DNA methylation.NAR genomics and bioinformatics · 2025Article
- RobusTAD: reference panel based annotation of nested topologically associating domains.Genome biology · 2025Article
- Rethinking GWAS: how lessons from genetic screens and artificial intelligence could reveal biological mechanisms.Bioinformatics (Oxford, England) · 2025Article
- CCCTC-binding factor regulates splicing factor proline and glutamine-rich to promote malignant growth of osteosarcoma.American journal of translational research · 2025Article
- Hidden secrets of the cancer genome: unlocking the impact of non-coding mutations in gene regulatory elements.Cellular and molecular life sciences : CMLS · 2024Review
- A germline point mutation in the MYC-FBW7 phosphodegron initiates hematopoietic malignancies.Genes & development · 2024Article
- RPL35A drives ovarian cancer progression by promoting the binding of YY1 to CTCF promoter.Journal of cellular and molecular medicine · 2024Article
- Spatial promoter-enhancer hubs in cancer: organization, regulation, and function.Trends in cancer · 2023Review
- Long-range gene regulation in hormone-dependent cancer.Nature reviews. Cancer · 2023Review
- Prominin 2 decreases cisplatin sensitivity in non-small cell lung cancer and is modulated by CTCC binding factor.Radiology and oncology · 2023Article
- Article
- MYC reshapes CTCF-mediated chromatin architecture in prostate cancer.Nature communications · 2023Article
- CRISPR/Cas9-mediated targeted knock-in of large constructs using nocodazole and RNase HII.Scientific reports · 2023Article
- SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023Review
- A global high-density chromatin interaction network reveals functional long-range and trans-chromosomal relationships.Genome biology · 2022Article
- Target-enriched nanopore sequencing and de novo assembly reveals co-occurrences of complex on-target genomic rearrangements induced by CRISPR-Cas9 in human cells.Genome research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundRecent genome-wide association studies (GWAS) have identified more than 100 loci associated with increased risk of prostate cancer, most of which are in non-coding regions of the genome. Understanding the function of these non-coding risk loci is critical to elucidate the genetic susceptibility to prostate cancer.
resultsWe generate genome-wide regulatory element maps and performed genome-wide chromosome confirmation capture assays (in situ Hi-C) in normal and tumorigenic prostate cells. Using this information, we annotate the regulatory potential of 2,181 fine-mapped prostate cancer risk-associated SNPs and predict a set of target genes that are regulated by prostate cancer risk-related H3K27Ac-mediated loops. We next identify prostate cancer risk-associated CTCF sites involved in long-range chromatin loops. We use CRISPR-mediated deletion to remove prostate cancer risk-associated CTCF anchor regions and the CTCF anchor regions looped to the prostate cancer risk-associated CTCF sites, and we observe up to 100-fold increases in expression of genes within the loops when the prostate cancer risk-associated CTCF anchor regions are deleted.
conclusionsWe identify GWAS risk loci involved in long-range loops that function to repress gene expression within chromatin loops. Our studies provide new insights into the genetic susceptibility to prostate cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.