We found that: (i) MED1 is necessary for ARv567es induced UBE2C up-regulation and subsequent prostate cancer cell growth; (ii) p-MED1 is recruited to ARv567es independent of full-length AR; (iii) p-MED1 has higher recruitment to UBE2C promoter and enhancer regions in the presence of ARv567es, (iv) ARv567es enhanced UBE2C transcription could be blocked by silencing MED1; (v) ARv567es/p-MED1 signaling crosstalks with the PI3K/AKT pathway but not the MAPK pathway, and (vi) FoxA1 is involved in ARv567es/p-MED1 induced UBE2C long range chromatin interactions. This evidence concerns the gene AKT1 and prostate cancer.