Prostate cancer (PCa) is initially sensitive to androgen deprivation therapy (ADT) but invariably develops into castration resistant PCa (CRPC) over time. Yet, CRPC remains dependent on androgen receptor (AR) signaling. Studies showed that androgen seems to have a biphasic role for PCa growth. The growth of human AR-positive both castration sensitive PCa (CSPC) and CRPC cell lines can be inhibited by supraphysiological androgen level (SAL).The bipolar androgen therapy (BAT) includes cycles of SAL under continuous ADT and is in clinical trial to treat CRPC patients. Interestingly, SAL induces cellular senescence in AR-positive PCa cells and ex vivo in PCa tumor patients’ samples. However, while AKT signaling plays a role in this pathway, the underlying mechanism of SAL induced senescence is not completely understood. This thesis shows for the first time that the cell cycle inhibitor p15INK4b is involved in SAL-induced cellular senescence in both CSPC LNCaP and CRPC C4-2 cells. Treatment with the AKT inhibitor (AKTi) potently inhibited SAL-induced expression of p15INK4b and cellular senescence in both cell lines. Transcriptome sequencing (RNA-seq) comparing the SAL-induced transcriptomes of LNCaP with C4-2 cells as well as of AKTi treated cells revealed landscapes for cell senescence. Interestingly, ANXA2 and lncRNA SAT1 are among identified genes. ANXA2 knockdown reduces the percentage of SAL induced senescent cells, which suggests the ANXA2 as a mediator of cellular senescence in PCa cells. Another identified gene is the lncRNA SAT1. SAL treatment of native patient tumor samples ex vivo results in up-regulation of lncRNA SAT1. This suggests that lncRNA SAT1 serves as a tumor suppressor with SAL. Further results also indicate that the lncRNA SAT1 is crucial for SAL-induced cancer cell senescence and being an upstream factor for p15INK4b. LncRNA SAT1 may have a positive feedback loop with AKT or be present in the AR-AKT complex.