GSE111913
Genome-wide map of cohesin positions in RT112 bladder cancer cells
Bladder cancer is one of the most common genitourinary malignancies worldwide. It is a heterogeneous disease at the clinical, pathological, and genetic levels.   In an exome-sequencing study of bladder cancer, we identified genes mutated in bladder cancer coding for proteins involved in chromatin modification, cell division, and DNA repair. STAG2, a constituent of the cohesin complex, was commonly mutated or lost, mainly in tumors of low stage or grade. Loss of STAG2 expression was often observed in genomically stable tumors, suggesting that STAG2 may act as a tumor suppressor through mechanisms other than chromosome segregation (Balbás-Martínez et al. 2013). In addition to mediating sister chromatid cohesion, cohesin plays a central role in DNA looping and organization of the genome into Topologically Associating Domains (TADs). Two variant cohesin complexes that contain either STAG1 or STAG2 are present in all cell type. Here we addressed their genome wide binding in bladder cancer cells. Overall design: ChIPseq of STAG1, STAG2 and SMC1a (common cohesin component) binding sites in chromatin from RT112 bladder cancer cells.