Project description:Lamin A/C proteins, major components of the nuclear lamina, are encoded by the LMNA gene. These proteins have multiple cellular functions. LMNA has implications in cancer; however, its mechanisms of dysregulation in cancer cells are not yet fully understood. Among the LMNA transcript variants, we focused on a spliced variant 6 (termed LMNA-V6), which contains unique 3 exons upstream of exon 1 of LMNA. In this study, after LMNA-V6 levels were modulated by overexpression or silencing in colon cancer HCT116 cells, gene expression profiles were measured using microarray analysis.
Project description:overexpression of tumour suppressor ZAR1 in HCT116 (HCT116 wt and HCT116 delp53) colon carcinoma cell line (EYFPemtpy and ZAR1EYFP), sorted by Aria for fluorescent cells, RNA isolation
Project description:Analysis of gene expression levels altered by stable gelsolin overexpression. Results provide important information of the modulation of various genes by gelsolin. Total RNA obtained from stable gelsolin-overexpressing HCT116 clones (C1, C2, C3, C8) as well as emtpy vector control HCT116 cell lines (V4, V5)
Project description:Alteration of gene expression profile due to Lmna knockout was studied in MEF. Total RNA obtained from Lmna +/+ MEF and Lmna -/- MEF were compared.
Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.
Project description:Over 180 LMNA gene mutations have been identified in human diseases including cardiac and skeletal myopathies, lipodystrophies, and premature aging syndromes. Postulated mechanisms by which these mutations result in different phenotypes include perturbation of normal nuclear structure and chromosome organization, and gene activity. We investigated whether a cardiomyopathic LMNA mutation, E161K, displayed abnormal gene expression. We compared the gene expression profile in the E161K LMNA-mutant heart to that of an end stage LMNA-normal heart. We compared the gene expression levels between two end-stage cardiomyopathic hearts in order to detect the gene expression differences more likely to reflect the LMNA mutation state. A region of left ventricle tissue that was grossly less fibrotic and contained cardiomyocytes of the LMNA-mutant heart was selected for RNA isolation. A region of a male heart that was also end-stage dilated cardiomyopathy, but LMNA-normal and also devoid of obvious fibrosis was selected for RNA isolation. Two technical replicates were performed for each sample, and data were analyzed using two different normalization strategies (Mas5 and RMA).
Project description:To reveal the changes of miRNAs levels in HCT116 cells with METTL14 overexpression, we employed miRNA microarray expression profiling in HCT116 human colon cancer cells stably expressing control vector or METTL14.