BO1 - Small RNA, Big Impact: miR-718 as a Metabolic Modulator
Abstract
Many diseases including cancers, psychiatric illnesses, and cardiovascular disease are now known to have an epigenetic component, where gene expression changes without a change in DNA sequence. One such mechanism, microRNAs (miRNAs), are short, untranslated RNA sequences that bind to roughly complementary messenger RNAs (mRNAs) of other genes to induce the degradation of those mRNAs, hence stopping the ability to make protein for those genes. If a miRNA’s expression increases, the mRNAs of target genes would decrease, which leads to disease. One little-studied miRNA, miR-718, is predicted to target over 600 genes’ mRNA molecules for degradation and notably is co-transcribed with an autism spectrum disorder candidate gene, IRAK1. IRAK1 increases in the cortex of autism spectrum disorder patients’ brains, which means miR-718 is also overexpressed. This makes sense considering one target of miR-718, PTEN, which regulates autophagy through the PI3K/AKT/MTOR pathway. Many of the predicted targets for miR-718 include genes that code for enzymes involved in catalytic activity (cellular respiration) and oxidoreductase activity. In theory, this means that cellular energetics are affected when miR-718 expression is altered. Therefore, we hypothesized that upregulating miR-718 expression would negatively impact cellular respiration. To test our hypothesis, we used the Seahorse metabolic analyzer along with mitochondrial stress, glycolytic stress, and glycolytic rate test kits. Our preliminary findings indicate upregulation of miR-718 decreases the cell’s ability to produce ATP and induced cellular stress. Our findings warrant further investigation into the role of miR-718 expression in cellular energetics and stress.
BO1 - Small RNA, Big Impact: miR-718 as a Metabolic Modulator
CASB 101
Many diseases including cancers, psychiatric illnesses, and cardiovascular disease are now known to have an epigenetic component, where gene expression changes without a change in DNA sequence. One such mechanism, microRNAs (miRNAs), are short, untranslated RNA sequences that bind to roughly complementary messenger RNAs (mRNAs) of other genes to induce the degradation of those mRNAs, hence stopping the ability to make protein for those genes. If a miRNA’s expression increases, the mRNAs of target genes would decrease, which leads to disease. One little-studied miRNA, miR-718, is predicted to target over 600 genes’ mRNA molecules for degradation and notably is co-transcribed with an autism spectrum disorder candidate gene, IRAK1. IRAK1 increases in the cortex of autism spectrum disorder patients’ brains, which means miR-718 is also overexpressed. This makes sense considering one target of miR-718, PTEN, which regulates autophagy through the PI3K/AKT/MTOR pathway. Many of the predicted targets for miR-718 include genes that code for enzymes involved in catalytic activity (cellular respiration) and oxidoreductase activity. In theory, this means that cellular energetics are affected when miR-718 expression is altered. Therefore, we hypothesized that upregulating miR-718 expression would negatively impact cellular respiration. To test our hypothesis, we used the Seahorse metabolic analyzer along with mitochondrial stress, glycolytic stress, and glycolytic rate test kits. Our preliminary findings indicate upregulation of miR-718 decreases the cell’s ability to produce ATP and induced cellular stress. Our findings warrant further investigation into the role of miR-718 expression in cellular energetics and stress.