BMB-7 MiR-718 impacts an epigenetic mark to regulate miR-132 expression: Implications in ASD and cancer
Abstract
MicroRNAs are known to be involved in disease etiologies for cancer, psychiatric illnesses, and others. One miRNA, miR-718, is of interest in Autism Spectrum Disorders (ASD) due to its location. The transcript of miR-718 overlaps with the transcript of the 5' UTR of the IRAK1 gene, which is known to be increased in ASD brains. Therefore, it is likely that miR-718 is also increased in ASD, yet this has not been discovered. A previous study found that the increased expression of miR-718 leads to the loss of autophagy and increased dendritic spines, which are characteristics of ASD. Additionally, an upregulation of miR-718 leads to the downregulation of miR-132, a miRNA that is decreased in ASD and schizophrenia. In this study, we are interested in discovering the mechanism underpinning the decrease in miR-132 with upregulation of miR-718 as we suspect it may be due to an epigenetic change around the promoter of miR-132.We performed a Chromatin Immunoprecipitation followed by qPCR (ChIP-qPCR) using an antibody for the histone modification H3K4me3, which is enriched around miR-132’s promoter. We designed primers around the miR-132 promoter and used RT-qPCR with SYBR Green to determine whether H3K4me3 levels were changed around miR-132. Our study could have major implications in our understanding of cellular pathways that contribute to ASD and several cancers since miR-718 upregulation is related to poor outcomes in several cancers.
Keywords
microRNAs, epigenetics, cancer, ASD, histone modification
BMB-7 MiR-718 impacts an epigenetic mark to regulate miR-132 expression: Implications in ASD and cancer
University Readiness Center Greatroom
MicroRNAs are known to be involved in disease etiologies for cancer, psychiatric illnesses, and others. One miRNA, miR-718, is of interest in Autism Spectrum Disorders (ASD) due to its location. The transcript of miR-718 overlaps with the transcript of the 5' UTR of the IRAK1 gene, which is known to be increased in ASD brains. Therefore, it is likely that miR-718 is also increased in ASD, yet this has not been discovered. A previous study found that the increased expression of miR-718 leads to the loss of autophagy and increased dendritic spines, which are characteristics of ASD. Additionally, an upregulation of miR-718 leads to the downregulation of miR-132, a miRNA that is decreased in ASD and schizophrenia. In this study, we are interested in discovering the mechanism underpinning the decrease in miR-132 with upregulation of miR-718 as we suspect it may be due to an epigenetic change around the promoter of miR-132.We performed a Chromatin Immunoprecipitation followed by qPCR (ChIP-qPCR) using an antibody for the histone modification H3K4me3, which is enriched around miR-132’s promoter. We designed primers around the miR-132 promoter and used RT-qPCR with SYBR Green to determine whether H3K4me3 levels were changed around miR-132. Our study could have major implications in our understanding of cellular pathways that contribute to ASD and several cancers since miR-718 upregulation is related to poor outcomes in several cancers.