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Genome-wide association studies (GWAS) have identified single nucleotidepolymorphisms (SNPs) associated with trait diversity and diseasesusceptibility, yet the functional properties of many genetic variants andtheir molecular interactions remains unclear. It has been hypothesized thatSNPs in microRNA binding sites may disrupt gene regulation by microRNAs(miRNAs), short non-coding RNAs that bind to mRNA and downregulate the targetgene. While a number of studies have been conducted to predict the location ofSNPs in miRNA binding sites, to date there has been no comprehensive analysisof how SNP variants may impact miRNA regulation of genes. Here we investigatethe functional properties of genetic variants and their effects on miRNAregulation of gene expression in cancer. Our analysis is motivated by thehypothesis that distinct alleles may cause differential binding (from miRNAs tomRNAs or from transcription factors to DNA) and change the expression of genes.We previously identified pathways--systems of genes conferring specific cellfunctions--that are dysregulated by miRNAs in cancer, by comparingmiRNA-pathway associations between healthy and tumor tissue. We draw on theseresults as a starting point to assess whether SNPs in genes on dysregulatedpathways are responsible for miRNA dysregulation of individual genes in tumors.Using an integrative analysis that incorporates miRNA expression, mRNAexpression, and SNP genotype data, we identify SNPs that appear to influencethe association between miRNAs and genes, which we term "regulatory QTLs(regQTLs)": loci whose alleles impact the regulation of genes by miRNAs. Wedescribe the method, apply it to analyze four cancer types (breast, liver,lung, prostate) using data from The Cancer Genome Atlas (TCGA), and provide atool to explore the findings.

Single nucleotide polymorphisms that modulate microRNA regulation of gene expression in tumors