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Human Cancer Biology |
Authors' Affiliations: 1 Departments of Urology and Pathology, Emory University School of Medicine, Atlanta, Georgia; 2 Prostate Cancer Research Laboratory, Department of Urology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; 3 Department of Urology, First Hospital of Xi'an Jiaotong University, Urology Institute of Xi'an Jiaotong University, Xi'an, Shaanxi, China; and 4 Laboratory of Molecular Oncology, Institute of Biotechnology, Beijing, China
Requests for reprints: Ruoxiang Wang, Department of Urology, Emory University School of Medicine, Suite B5103, 1365B Clifton Road Northeast, Atlanta, GA 30322. Phone: 404-778-5116; Fax: 404-778-3965; E-mail: rwang2{at}emory.edu.
Purpose: We previously reported the isolation and characterization of PrLZ, a novel prostate-specific and androgen-responsive gene of the tumor protein D52 family at chromosome 8q21.1. PrLZ is the only known gene in this locus with prostate specificity. Expression level of PrLZ was elevated specifically in cancer cells, suggesting its association with malignancy.
Experimental Design: To define its biological function in the morphogenesis, development, and functional maturation of the prostate gland and to gain further insight into its role in prostate cancer, we examined PrLZ expression in prostate specimens during early embryonic development and in adult tissue.
Results: PrLZ first appears in the nuclei of the prostate epithelia at 16 weeks of gestation before its distribution in the cytoplasm at later ages. Its expression peaks at 24 years of age, declines at 31 years of age, and maintains a minimal level in later age. On prostate cancer development, PrLZ expression is reactivated, and its expression increases from primary localized tumor to bone metastasis. Overexpression of PrLZ in prostate cancer cells accelerates their growth in vitro and tumor formation in vivo.
Conclusion: This work identifies PrLZ as a marker for prostate cancer progression and metastasis, and its pattern of expression is suggestive of a proto-oncogene.
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