Prostate Cancer (PCa) is the second leading cause of cancer death in American men; one in six will be diagnosed with the disease during his lifetime. The androgen receptor (AR) is a transcription factor necessary for normal prostate cell growth as well as for growth of PCa. When AR is activated by androgens, it translocates to the nucleus and exerts transcriptional activation and repression of target genes. Significant efforts have focused on characterizing genes that are activated by AR such as prostate specific antigen (PSA), a marker for PCa screening. Genes that are transcriptionally repressed by AR are also likely to play a role in the progression of prostate cancer, yet the mechanisms behind their repression have received less attention. One such gene is maspin, a tumor suppressor gene that is repressed by androgens. Maspin expression is associated with increased cellular adhesion, increased sensitivity to cellular apoptosis, and decreased angiogenesis in the tumor microenvironment. In this study, we demonstrated that (1) Maspin is repressed following androgen treatment, (2) the repression is mediated in a direct manner, and (3) Androgen antagonists such as bicalutamide do not affect the ability of AR to repress maspin. Ongoing research will continue to investigate AR’s role in the repression of maspin. Understanding the underlying mechanisms by which AR represses maspin and other target genes may reveal novel opportunities for developing new prostate cancer therapies.
Additional contributor: Scott Dehm (faculty mentor).
Mechanisms of Androgen-Mediated Repression of the Maspin Tumor Suppressor Gene in Prostate Cancer.
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