[Molecular targeted therapy for prostate cancer]

Abstract

Androgen plays an important role in the growth of prostate cancer, but the molecular mechanism that underlies the development of resistance to anti-androgen therapy remains unknown. In this paper, we review the role of cell cycle regulators and steroid receptor co-activators for prostate cancer growth and survival. Cyclin E has been shown to increase the transactivation activity of the human androgen receptor and the proliferation of prostate cancer cells. On the other hand, p27 using an adenovirus vector was shown to reduce the size of tumors of human prostate cancer xenografts. Steroid receptor coactivator-3 (SRC-3) is often over-expressed in prostate cancers. Our results indicate that overexpression of SRC-3 can modulate the AKT (protein kinase B) signaling pathway and stimulate cell growth in prostate cancer. In contrast, down-regulation of SRC-3 expression by small interfering RNA suppresses cell growth.