The core SPOP<sup>MT</sup>;MYC<sup>High</sup> transcriptomic response, defined by the overlap between the SPOP<sup>MT</sup> and c-MYC transcriptomic programmes, was also associated with inferior clinical outcome in human PCs.
Indeed, we found that wild-type (wt) but not prostate adenocarcinoma-associated mutants of SPOP promoted AR ubiquitination and degradation, acting directly through a SPOP-binding motif in the hinge region of AR.