Interleukin-17 Receptor-like Gene is a Novel Antiapoptotic Gene Highly Expressed in Androgen-independent Prostate Cancer.
From: Center for Tissue Regeneration and Repair, Department of Orthopaedic Surgery, School of Medicine, University of California, Davis, Sacramento, California 95817, USA. zyou@ucdavis.edu
Cancer research
- Publish Date: Jan 2006
- ISSN: 0008-5472
- Volume: 66
- Issue: 1
- Pages: 175-83
- Medium: Print
- Language: English
- Citation (JAMA): You Zongbing, Shi Xu-Bao, DuRaine Grayson, et al. Interleukin-17 Receptor-like Gene is a Novel Antiapoptotic Gene Highly Expressed in Androgen-independent Prostate Cancer.. Cancer Res. Jan 2006;66:175-83
Abstract
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 alpha (TNFalpha)-sensitive LNCaP cells inhibited TNFalpha-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.
Mesh Headings (Keywords): Animals, Apoptosis, Caspases, Cell Adhesion, Cell Line, Tumor, Drug Resistance, Neoplasm, Enzyme Activation, Extracellular Matrix, Humans, Isoenzymes, Male, Mice, Mice, Nude, Neoplasms, Hormone-Dependent, Prostatic Neoplasms, RNA, Small Interfering, Receptors, Interleukin, Tumor Necrosis Factor-alpha
Check for Full Text / PubMed Unique Identifier (PMID): 16397230
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