MCF7 ChIP-seq
LCOR is a corepressor of activated nuclear receptors that inhibits the transcriptional activity of these proteins. Recently, LCOR was described to act also as a transcription activator by DNA direct binding through its HTH domain of genes involved in antigen presentation. This double transcriptional role of LCOR is determined by the expression of nuclear receptor. Here we performed ChiP-seq analysis of LCOR in MCF-7 cells which expressed the nuclear receptor estrogen receptor. In paralel we treated the cells with an estrogen receptor degrader (fulvestrant) or ectopic expression of the LCOR without the nuclear receptor binding domain (LSKAA). This analysis allows to compare the genome wide distribution of LCOR depending on the presence of nuclear receptor and the ability to interact. Overall design: MCF7 cells were transduced with control, LCOR and LSKAA inducible overexpressing plasmids. MCF7-LCOR OE cells were induced with 1 ug/ml of doxycycline and treated with vehicle or 1 uM of fulvestrant. MCF7-LSKAA OE were induced with doxycycline. After 24 h, cells were croslinked and chromatin extracts were obtained for immunoprecipitation of LCOR. Isolated DNA bound to LCOR was submitted for sequencing. After alignment and analysis of sequenced DNA, conditions were compared to check the different prefferentially bound motif of LCOR in each condition