GSE132716
Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - ChIPseq data
In order to identify direct gene targets and pathways regulated by MEIS1 in prostate cells and identify mechanisms of observed tumor suppression with MEIS1 expression, we performed Chromatin Immunoprecipitation and sequencing (ChIP-seq) of MEIS1 in the CWR22Rv1-LV-MEIS1 line. Also, given the dependence of HOXB13, and to enable determination of HOXB13-dependent vs. HOXB13-independent MEIS1 DNA binding, we performed parallel MEIS1 ChIP-seq in the CWR22Rv1-HOXB13ko-LV-MEIS1 line.  LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. Knockout of HOXB13 was achieved by CRISPR and validated with western blotting. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cells, so these cells are positive for MEIS1 expression and negative for HOXB13. Overall design: MEIS1 immunoprecipitation was performed in triplicate for the LV-MEIS1 condition and was performed in duplicate for the HOXB13ko-LV-MEIS1 condition. Non-immunoprecipitated DNA was used as an input DNA control when calling peaks. Replicates in each condition were pooled using MACS2 to call peaks against the input DNA control.