Identification of differential expressed genes of JQ1 or JQ1+Bortezomib in colorectal cancer cells

The bromodomain and extra-terminal domain inhibitors (BETi) are promising epigenetic drugs for the treatment of various cancers through suppression of oncogenic transcription factors including MYC. However, only a subset of CRC cells response to BETi, suggesting an intrinsic resistance to BETi in CRC. We investigated the effect of JQ1 on cell proliferation, apoptosis, angiogenesis and MYC expression in a panel of 11 CRC cells in vitro and in vivo. JQ1-resistant CRC cells were used for the screening for the effective combination therapies with JQ1. RNA-seq of single drug or combined drugs treatment was performed to explore the mechanism of action. Overall design: RKO cells were treated with JQ1 (1 µM) for 6 h. HCT116 cells were treated with DMSO, JQ1 (1 µM) , Bortezomib (5nM), JQ1 (1 µM)+Bortezomib (5nM) for 6h. RNA was extracted for RNA-seq.