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Signaling and Regulation

Regulation of IB Kinase Expression by the Androgen Receptor and the Nuclear Factor-B Transcription Factor in Prostate Cancer

¹ Centre de Recherche du Centre Hospitalier de l'Université de Montréal/Institut du cancer de Montréal; ² Département de Médecine de l'Université de Montréal; ³ Département de Chirurgie de l'Hôpital Notre-Dame (Centre Hospitalier de l'Université de Montréal), Montréal, Quebéc, Canada

Requests for reprints: Anne-Marie Mes-Masson, Centre de Recherche du Centre Hospitalier de l'Université de Montréal/Institut du cancer de Montréal, 1560 rue Sherbrooke Est (Y-4609), Montréal, Québec, Canada H2L 4M1. Phone: 514-890-8000, ext. 25496; Fax: 514-412-7703. E-mail: anne-marie.mes-masson{at}umontreal.ca

Although several genes have been associated with prostate cancer progression, it is clear that we are far from understanding all the molecular events implicated in the initiation and progression of the disease to a hormone-refractory state. The androgen receptor is a central player in the initiation and proliferation of prostate cancer and its response to hormone therapy. Nuclear factor-B has important proliferative and antiapoptotic activities that could contribute to the development and progression of cancer cells as well as resistance to therapy. In this study, we report that IB kinase (IKK), which is controlled by nuclear factor-B in human chondrocytes, is expressed in human prostate cancer cells. We show that IKK gene expression is stimulated by tumor necrosis factor- treatment in LNCaP cells and is inhibited by transfection of a dominant-negative form of IB, which prevents the nuclear translocation of p65. Furthermore, we found that tumor necrosis factor-–induced IKK expression is inhibited by an androgen analogue (R1881) in androgen-sensitive prostate cancer cells and that this inhibition correlates with the modulation of IB expression by R1881. We also noted constitutive IKK expression in androgen-independent PC-3 and DU145 cells. To our knowledge, this is the first report of an IB kinase family member whose expression is modulated by androgen and deregulated in androgen receptor–negative cells. (Mol Cancer Res 2007;5(1):87–94)

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