Effect of USP10 knockout using CRISPR on gene expression in MCF7 breast cancer cells

Using a genome wide shRNa screen we identified the deubiqutinating enzyme USP10 as a potent regualtor of AKT activity. To validate our findings we performed RNA-Seq on MCF7 cells with or without USP10 depletion. In line with our previous observations we demonstrate that PI3k-AKT-mTOR pathway activation is downregualted in our USP10 knockout cells. Our later work shows that this function is mediated through a USP10-GSK3B mediated mechanism resulting in PTEN inactivation. Taken together this work demonstrates the imprtance of USP10 in PI3K pathway regualtion. Overall design: RNA-Seq profiling of wildtype MCF7 cells and their USP10 knockout counterparts. Cells were taken from 5 sequential replicates.