Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. Using a CRISPR/Cas9 approach, we generated three STAG2 knock-out isogenic clones (A673SA2m#1, TC71SA2m#1 and TC71SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. A STAG2 rescue model (A673_SA2r) generated by correcting the CRISPR mutation in the A673SA2m#1 model was also profiled using RNA-seq. Comparison of RNA-seq data allowed highlighting a broad transcriptional modulation upon STAG2 knock-out. In addition, we compared these analyses with STAG1 knock-out A673 derived model (A673SA1m#1) and with A673 (WT) and TC71 (WT) parental cells lines transfected with siCT or siEWS-FLI1.
Project description:We report the transcriptional difference of LATS1/2 gene knock out T47D cells with wild type control using RNA-seq technology. We further generated the chromatin binding of multiple proteins, including YAP, TEAD2, Estrogen receptor alpha, VGLL3 and several histone marks, as well as ATAC profiling between LATS1/2 gene knock out MCF7 cells with wild type control.