Enhanced DR5 induction was necessary for the chemosensitization and apoptotic effects of BETi and was responsible for increased BETi sensitivity in colorectal cancer cells containing a mutation in speckle-type POZ protein (<i>SPOP</i>), a subunit of BRD4 E3 ubiquitin ligase.
Silencing speckle-type POZ protein by promoter hypermethylation decreases cell apoptosis through upregulating Hedgehog signaling pathway in colorectal cancer.
Our results suggest that SPOP plays a pivotal role in colorectal cancer (CRC) through mesenchymal-epithelial transition and MMPs, and it may be a potential therapeutic target in colorectal cancer.