Prostate cancer relies on the male hormone androgen for growth and survival. The action of androgens in the prostate is mediated by its cognate receptor, the androgen receptor (AR), which is a transcription factor that binds to promoters and enhancers to activate or repress gene transcription. The importance of the AR in prostate cancer is highlighted by therapeutic targeting using anti-androgens such as bicalutamide (Astrazenica) and enzalutamide (Medivation), however many tumours eventually progress to an anti-androgen resistant state.  Here, we use RNAseq to detect 71 high-confidence fusion transcripts that are expressed in the LNCaP prostate cancer cell line after treatment with androgen (DHT) or anti-androgen drugs (bicalutamide and enzalutamide). Most of these fusion transcripts result from ‘read-through’ transcription of adjacent genes, with the distances between fusion transcripts originating from two genes that are located on the same chromosome varying between 0.4 kilobases to 61 megabases. Inspection of ChIPseq profiles indicated that there is an increase in AR occupancy around fusion transcript loci after androgen treatment, suggesting that the AR plays a role in mediating fusion transcription. Using clinical RNAseq data, we also found that a number of the androgen and anti-androgen regulated fusion transcripts were differentially expressed in prostate cancers compared to normal adjacent tissue. Collectively, we conclude that fusion transcripts might reflect a novel mechanism adopted by prostate cancer cells as they acquire treatment resistance to anti-androgen therapy.