Project description:Telomere dysfunction is the most common identifiable cause of pulmonary fibrosis. Cellular senescence of epithlial cells is thought to play a signfiicant role in disease pathogensis. We established a model of cellular senescence using a human alveolar epithelilial-like cell lines (A549) and profiled the transcriptional changes that occur in response to telomere dyfunction. Telomere dysfunction was induced by expressing a dominant-negative form TRF2, the shelterin binding protein.
Project description:RNA-sequencing of proliferating, doxorubicin-induced senescent, palbociclib (CDK4/6i)-induced senescent and INK128-induced diapause-like human melanoma SK-Mel-103 cells and human NSCLC A549
Project description:In this study we transfected A549 cells with siRNA against TNFAIP2, infected them with L. pneumophila and performed transcriptional profiling. We found enrichment of genes in pro-inflammatory pathways by Pathway Over-respresentation analysis upon infection. There was no significant change in gene expression that we could attribute specifically to the knockdown of TNFAIP2. Examination of the transcriptional response of A549 cells to Legionella infection with concomitant TNFAIP2 knockdown