Project description:RNA-sequencing of senescent (doxorubicin) human melanoma SK-MEL-103 cells and human fetal lung fibroblast IMR-90 with different interventions
Project description:Analysis of gene expression profile in Ras-induced senescent human diploid fibroblasts with or without depletion of fzr1/cdh1. Results provide insight into the effect on fzr1/cdh1 on the regulation of senescence-associated gene expression in human diploid fibroblasts. IMR-90-ER:Ras cells were cultured for 6 days with or without 4-hydroxytamoxifen (OHT) and were subsequently subjected to transfection with siRNA oligos against fzr1/cdh1 or control for three times (at 2 day intervals). Total RNA was isolated using Trizol reagent and were analyzed using the human 3D-Gene DNA chip (Toray) which that contains 25000 genes. The genome wide transcriptional response of proliferating cells (IMR si control2) and fzr1/cdh1 depleted senescent cells (IMR+OHT si cdh1) were compared to that of senescent cells (IMR+OHT si control).
Project description:Comparisong of gene expression of human IMR-90 at 27 and 55 population doublings. RNA-seq data comprises 2 groups: 27 and 55 population doublings of IMR-90. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:ChIP-seq analysis of NSD2 in IMR-90 cells. We found that NSD2 is enriched at gene bodies of actively transcribed genes and required for maintenace of H3K36me3 levels at these loci.
Project description:Abstract: Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage, and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage, and β-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across 8 diverse models of senescence triggered in human diploid fibroblasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V. The intersection of the altered transcriptomes revealed 47 RNAs consistently elevated and 26 RNAs consistently reduced across all senescence models, including many protein-coding mRNAs and some long noncoding RNAs. We propose that these shared transcriptome profiles will enable the identification of senescent cells in vivo, the investigation of their roles in aging and malignancy, and the development of strategies to target senescent cells therapeutically.
