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Interleukin-17 Receptor-Like Gene Is a Novel Antiapoptotic Gene Highly Expressed in Androgen-Independent Prostate Cancer

¹ Center for Tissue Regeneration and Repair, Department of Orthopaedic Surgery; Departments of ² Urology and Cancer Center, ³ Biochemistry and Molecular Medicine and Cancer Center, and ⁴ Pathology, School of Medicine, University of California, Davis, Sacramento, California

Requests for reprints: Zongbing You, Center for Tissue Regeneration and Repair, Department of Orthopaedic Surgery, School of Medicine, University of California, Davis, Room 2000, 4635 Second Avenue, Sacramento, CA 95817. Phone: 916-734-5750; Fax: 916-734-5750; E-mail: zyou{at}ucdavis.edu.

We have recently identified a new gene, interleukin-17 receptor-like (IL-17RL), which is expressed in normal prostate and prostate cancer. This investigation is focused on the role of IL-17RL in prostate cancer. We found that IL-17RL was expressed at significantly higher levels in several androgen-independent prostate cancer cell lines (PC3, DU145, cds1, cds2, and cds3) and tumors compared with the androgen-dependent cell lines (LNCaP and MLC-SV40) and tumors. In an in vivo model of human prostate tumor growth in nude mice (CWR22 xenograft model), IL-17RL expression in tumors was induced by androgen deprivation. The relapsed androgen-independent tumors expressed higher levels of IL-17RL compared with the androgen-dependent tumors. Overexpression of IL-17RL in tumor necrosis factor (TNF)–sensitive LNCaP cells inhibited TNF-induced apoptosis by blocking activation of caspase-3 downstream to caspase-2 and caspase-8. Reciprocally, knocking down IL-17RL expression by small interfering RNA induced apoptosis in all the prostate cancer cell lines studied. Taken together, these results show that IL-17RL is a novel antiapoptotic gene, which may confer partially the property of androgen-independent growth of prostate cancer by promoting cell survival. Thus, IL-17RL is a potential therapeutic target in the treatment of prostate cancer. (Cancer Res 2006; 66(1): 175-83)

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