Discipline: Biological Sciences
Subcategory: Cancer Research
Brianna Brantley - Clark Atlanta University
Co-Author(s): Aisha Hunt and Jaideep Chaudhary, Clark Atlanta University, Atlanta, GA
Single Nucleotide Polymorphism (SNP’s), are variations in a DNA sequence that transpire when a single nucleotide in the genome is different from the members of biological species or paired chromosomes. SNPs have the ability to alter the function of a protein, regulate genes, and cause variations in humans. SNPs come in two forms; synonymous and non-synonymous. Nonsynonymous SNPs change the amino acid in the translated protein and thus the function of the protein, while synonymous SNPs do not. Our ultimate objective is to understand if nonsynonymous SNPs alter genetic function and increase disease elements of ID4 in prostate cancer. Inhibitor of DNA binding protein 4 (ID4) is the dominant negative regulator of basic helix loop helix (bHLH) family of transcription factors. ID4 shares the homology of the HLH domain with other IDs and lack the basic DNA binding region. Unlike ID1, ID2 and ID3, ID4 acts as a tumor suppressor in prostate cancer by attenuating cell proliferation and promoting apoptosis. ID4 is epigenetically silenced in prostate cancer due to promoter hyper methylation, but it is expressed in some prostate cancer specimen and cell lines such as PC3. Although ID4 could be present, it may be nonfunctional due to the presence of nonsynonymous SNP’s in the highly conserved region of the HLH domain. This led us to hypothesize that non-synonymous such as rs1320311, rs1252783, rs7772056, rs7753263, rs6906699, rs1047033, rs1047014, and rs932346 serve as markers in establishing ID4 as a susceptibility loci in African-American and Japanese/Latino populations. Therefore, non-synonymous SNP’s around ID4 could be associated with increased risk of Prostate Cancer. We used a publicly available database known as GWAS (Genome Wide Association Studies) to analyze association between ID4 SNPs in prostate cancer. The study we selected was the Multiethnic Genome-wide Scan of Prostate Cancer, which contained 2,841 African-American samples (1,343 cases and 1,498 controls) and 1,660 Japanese/Latino samples (834 cases and 826 controls). Then, we used PLINK, a whole genome association analysis toolset, to analyze the genomes. PLINK software mainly focuses on the analysis of genotype/phenotype data which has the ability to extract frequencies on the SNPs in association with prostate cancer.
Funder Acknowledgement(s): NIH/NIMHD, Grant # 5 P20 MD002285
Faculty Advisor: Jaideep Chaudhary,