Over-expression of FLI1 in the epithelial cell line HaCaT increased expression of inflammatory markers associated with psoriasis

Friend virus induced leukemia-1 (Fli-1) is a ETS related oncogenic transcription factor initially identified by our group as a target of retroviral insertional mutagenesis in erythroleukemia induced by Friend virus. This oncogene is also activated through translocation (EWS-FLI1) or overexpression in various human solid and liquid tumors. In addition to cancer, FLI1 is involved in the development of various illnesses including inflammatory diseases. While overexpression of Fli-1 contributes to the development of autoimmune systemic lupus erythematosus (SLE), loss of this transcription factor in fibroblasts underlines systemic sclerosis. Finally, Fli-1 is also a major regulator of immunity, hematopoiesis and stem cell maintenance and developmen. Previously, we used RNAseq data of FLI1-depleted human leukemic cells and identified a correlation between FLI1 deficiency and reduced expression of markers of psoriasis. Accordingly, overexpression of FLI1 in the epithelial cell line HaCaT increased expression of these markers of inflammation and psoriasis. Overall design: To investigate the tight correlation between expression of FLI1 and inflammatory genes associated with psoriasis, over-expression of FLI1 was performed in the epithelial cell line HaCaT. Gene expression profiling analysis was conducted using data obtained from RNA-seq of the two cell types. Comparative gene expression profiling analysis was then performed on the RNA-seq data for the control HaCaT cell (Migr1) and the HaCaT-FLI1 cell (MigrFLI1)