ArticleMolecular and cellular biology2010
Upregulation of c-MYC in cis through a large chromatin loop linked to a cancer risk-associated single-nucleotide polymorphism in colorectal cancer cells.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 5 of them syntheses that pooled it.
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Who cites it
155 citing papers in PubMed, 5 syntheses or guidelines pooled it, 267 citations in OpenAlex.
- The landscape of GWAS validation; systematic review identifying 309 validated non-coding variants across 130 human diseases.BMC medical genomics · 2022Pooled it
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- Fine-scale mapping of 8q24 locus identifies multiple independent risk variants for breast cancer.International journal of cancer · 2016Pooled it
- Networks of intergenic long-range enhancers and snpRNAs drive castration-resistant phenotype of prostate cancer and contribute to pathogenesis of multiple common human disorders.Cell cycle (Georgetown, Tex.) · 2011Pooled it
- PLAAT2 suppresses gastric cancer progression by facilitating cMyc ubiquitination and inhibiting MEK/ERK signaling.Cell death & disease · 2026Article
- Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Harnessing the LncRNA CCAT2 role in gastric cancer: from molecular insights to clinical implications.Cancer cell international · 2026Review
- Dissecting regulatory non-coding GWAS loci reveals fibroblast causal genes with pathophysiological relevance to heart failure.Nature communications · 2025Article
- Accurate Measurement of Cell Number-Normalized Differential Gene Expression in Cells Treated With Retinoic Acid.Bio-protocol · 2024Article
- Melatonin and cancer suppression: insights into its effects on DNA methylation.Cellular & molecular biology letters · 2022Article
- Transposon-activated POU5F1B promotes colorectal cancer growth and metastasis.Nature communications · 2022Article
- CASCADE: high-throughput characterization of regulatory complex binding altered by non-coding variants.Cell genomics · 2022Article
- Integrating Multimorbidity into a Whole-Body Understanding of Disease Using Spatial Genomics.Results and problems in cell differentiation · 2022Article
- Chromatin Immunoprecipitation Assays on Medulloblastoma Cell Line DAOY.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The Roles of the Colon Cancer Associated Transcript 2 (CCAT2) Long Non-Coding RNA in Cancer: A Comprehensive Characterization of the Tumorigenic and Molecular Functions.International journal of molecular sciences · 2021Review
- Decoding the Equine Genome: Lessons from ENCODE.Genes · 2021Review
- A nuclear polymorphism at the 8q24 region is associated with improved survival time and chemo-response in high-grade serous ovarian cancer.Oncology letters · 2021Article
- Characterization and clinical evaluation of microsatellite instability and loss of heterozygosity within tumor-related genes in colorectal cancer.BMC medical genomics · 2021Article
- Wnt target enhancer regulation by a CDX/TCF transcription factor collective and a novel DNA motif.Nucleic acids research · 2021Article
95 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genome-wide association studies have mapped many single-nucleotide polymorphisms (SNPs) that are linked to cancer risk, but the mechanism by which most SNPs promote cancer remains undefined. The rs6983267 SNP at 8q24 has been associated with many cancers, yet the SNP falls 335 kb from the nearest gene, c-MYC. We show that the beta-catenin-TCF4 transcription factor complex binds preferentially to the cancer risk-associated rs6983267(G) allele in colon cancer cells. We also show that the rs6983267 SNP has enhancer-related histone marks and can form a 335-kb chromatin loop to interact with the c-MYC promoter. Finally, we show that the SNP has no effect on the efficiency of chromatin looping to the c-MYC promoter but that the cancer risk-associated SNP enhances the expression of the linked c-MYC allele. Thus, cancer risk is a direct consequence of elevated c-MYC expression from increased distal enhancer activity and not from reorganization/creation of the large chromatin loop. The findings of these studies support a mechanism for intergenic SNPs that can promote cancer through the regulation of distal genes by utilizing preexisting large chromatin loops.
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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.