Project description:We report a mutant mouse in which the uORF encoded by the PPARGC1A gene is disrupted via mutation of its start codon (uORF-TAA mutation). RNA-seq was used to assess differential gene expression in uORF-TAA versus wild-type mice in two metabolically important tissues that express PPARGC1A: skeletal mucle and brown adipose tissue.
Project description:LncRNAs play a crucial role in regulating the progression of NSCLC, making them potential targets for cancer diagnosis and treatment. Therefore, identifying new lncRNAs as therapeutic target and comprehending their underlying regulatory mechanisms are crucial for treating NSCLC. In this study, we found that glioblastoma down-regulated RNA (GLIDR) was increased in non-response NSCLC patients with the primary treatment, and GLIDR was also highly expressed in NSCLC patients. We used bioinformatic analysis and luciferase assays to identify that microRNA-342-5p (miR-342-5p) directly targets GLIDR. MiR-342-5p overexpression inhibits NSCLC cell proliferation, migration, and invasion, whereas miR-342-5p inhibition promotes NSCLC malignancy, which can be rescued by suppressing GLIDR. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PPARGC1A) was identified as a downstream target of miR-342-5p. PPARGC1A inhibition significantly suppresses NSCLC malignancy, whereas overexpression promotes it. The results also revealed that GLIDR overexpression reduced PPARGC1A inhibition by miR-342-5p, and increased PPARGC1A expression reversed the inhibition of NSCLC malignancies caused by decreased GLIDR. To the best of our knowledge, we are the first to discover that GLIDR promotes NSCLC progression by sponging miR-342-5p to regulate PPARGC1A expression, presenting that GLIDR act as a potential therapeutic target in NSCLC.
Project description:PPARGC1A oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. We generated gene-expression profile of control and PPARGC1A suppressed A549 cells, a lung adenocarcinoma cell line that expresses moderate levels of PPARGC1A to investigate the role of this gene in lung cancer metastasis.
Project description:We report the application of single cell RNAseq assay in examining the effect of Ppargc1a gene expression in intestinal stem cells on mucosal homeostasis. Lgr5EGFPcreERT2 mice were crossed with Ppargc1a F/+ or F/F to selectively target gene expression in Lgr5 expressing intestinal stem cells. Mice were fed with control diet AIN76A from weaning for 3 months, and deletion of Ppargc1a gene was conducted via Tamoxifen injection. Mice were sacrificed 3 days post tamoxifen injection.
Project description:Transgenic mice overexpressing a novel regulator of mitochondrial dynamics, transmembrane protein 135 (Tmem135) have age-related heart phenotypes. Here we report the gene expression profiles of 6 mo old WT and Tg whole hearts. RNAseq was conducted on Illumina HiSeq 2000 platform.
Project description:To determine genes regulated by the transcriptional co-activator PPARGC1A in OAC cells and whether PPARGC1A activity is altered by lapatinib we performed RNA-seq on OE19 cells treated with non-targeting siRNA or siRNA targeting PPARGC1A. 24 hours post-transfection, cells were also treated with either DMSO or 500 nM lapatinib for 24 hours.
Project description:Analysis of ventricular derived mRNA from cardiac specific Cdk8 overexpressing mice. Results provide insight into the molecular mechanisms underlying dilated cardiomyopathy and heart failure.