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. Author manuscript; available in PMC: 2019 May 20.
Published in final edited form as: Sci Signal. 2018 Nov 20;11(557):eaau7632. doi: 10.1126/scisignal.aau7632

Fig. 3. siRNA-mediated knockdown of HDAC and gene expression and PAX3:FOXO1 binding data for key aRMS gene targets.

Fig. 3.

(A and B) PAX3:FOXO1 expression in Rh30 cells transfected with siRNA at 100 nM for 72 hours targeting HDAC1, HDAC2, and/or HDAC3 (A), as well as HDAC10 (B). Blots are representative of N=3 independent experiments. (C-F) Three aRMS samples [U23674 in two replicates (U23674A and U23674B), Rh30, and Rh41] were sequenced after treatment with ENT at 2 μM for 72 hours or DMSO. Featured genes were decreased (log2 ratio of ENT-induced expression divided by control expression > 1) in all samples. Additional expression data for these key targets were curated from previous publications (10, 33) and PAX3:FOXO1 binding data was curated from the literature as indicated (31, 32) or was generated through ChIP-Seq experiments. Four subclasses of ENT-induced gene expression were identified as (C) PAX3:FOXO1 binding with or without HDAC binding, (D) HDAC1, 2, 3 or 11 binding only, (E) indirect targets of PAX3:FOXO1, and (F) otherwise-regulated genes.