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The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression
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The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression
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Journal Article
The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression
2017
Overview
Genome-wide association studies have identified a great number of non-coding risk variants for colorectal cancer (CRC). To date, the majority of these variants have not been functionally studied. Identification of allele-specific transcription factor (TF) binding is of great importance to understand regulatory consequences of such variants. A recently developed proteome-wide analysis of disease-associated SNPs (PWAS) enables identification of TF-DNA interactions in an unbiased manner. Here we perform a large-scale PWAS study to comprehensively characterize TF-binding landscape that is associated with CRC, which identifies 731 allele-specific TF binding at 116 CRC risk loci. This screen identifies the A-allele of rs1800734 within the promoter region of
MLH1
as perturbing the binding of TFAP4 and consequently increasing
DCLK3
expression through a long-range interaction, which promotes cancer malignancy through enhancing expression of the genes related to epithelial-to-mesenchymal transition.
Functional characterisation of non-coding risk variants for colorectal cancer is missing. Here the authors conduct a large-scale proteome-wide analysis of disease associated SNPs to characterize allele-specific transcription factor binding landscape in colorectal cancer and identify one functionally significant SNP.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 42/109
/ 82/58
/ Alleles
/ Colonic Neoplasms - genetics
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - metabolism
/ Genes
/ Genetic Predisposition to Disease
/ Genome-Wide Association Study
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ Intracellular Signaling Peptides and Proteins - genetics
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Mutation
/ MutL Protein Homolog 1 - genetics
/ Polymorphism, Single Nucleotide
/ Protein Serine-Threonine Kinases - genetics
/ Protein Serine-Threonine Kinases - metabolism
/ Proteome
/ Science
