Importantly, our data provide new mechanisms showing that MEN1 silencing led to the prominent nuclear translocation of JunD, which resulted not only in its increased binding to the regulatory sequence of the MYC locus, thus maintain MYC expression, but also in the altered expression of EMT markers, contributing to the aggravated tumorigenic potential seen in these MEN1-KD AR-independent PCa cells. Here, AR is linked to posterior cortical atrophy.