Fig. 3
From: Preclinical rationale for entinostat in embryonal rhabdomyosarcoma
CRISPR/Cas9 mediated HDAC3 inhibition and evaluation of tumor cell growth inhibition in eRMS and HDAC1/2/3/11 binding data for key ENT-treated eRMS samples. a CRISPR/Cas9 screen for the viability of selected HDAC3 excision by CRISPR in murine eRMS. b RNA from four human and murine eRMS cultures (U37125 in two replicates, U57810, RD, RH18) were sequenced following ENT treatment at 2 μM for 72 h and compared against DMSO-treated cultures. Rh18 which was hypersensitive to ENT and was only treated for 24 h. Key hits were identified as those overexpressed (log2 ratio of ENT expression divided by control expression > 1) in all samples