A positive role of c-myc in regulating androgen receptor and its splice variants in prostate cancer
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The androgen receptor (AR) is the main therapeutic target in prostate cancer. Androgen deprivation therapy, the first-line treatment for advanced prostate cancer, disrupts AR signaling by decreasing androgen levels or by inhibiting AR activity with AR antagonists
Androgens and androgen receptors (AR) regulate normal prostate development and growth. They also are involved in pathological development of prostatic diseases, including benign prostatic hyperplasia (BPH) and prostate cancer (PCa). Antiandrogen therapy for PCa, in conjunction with chemical or surgical castration, offers initial positive responses and leads to massive prostate cell death. However, cancer cells later appear as androgen-independent PCa. To investigate the role of AR in prostate cell proliferation and survival, we introduced a vector-based small interfering RNA (siRNA). This siRNA targeted 5'-untranslated region of AR mRNA for extended suppression of AR expression in androgen-sensitive human prostate LNCaP cells.