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Adenovirus-Mediated Overexpression of REIC/Dkk-3 Selectively Induces Apoptosis in Human Prostate Cancer Cells through Activation of c-Jun-NH₂-Kinase

Departments of ¹ Cell Biology and ² Urology, Okayama University Graduate School of Medicine and Dentistry, Okayama; and ³ Niimi College, Niimi, Japan

Requests for reprints: Nam-ho Huh, Department of Cell Biology, Okayama University Graduate School of Medicine and Dentistry, Shikatachou, Okayama 700-8558, Japan. Phone: 81-86-235-7393; Fax: 81-86-235-7400; E-mail: namu{at}md.okayama-u.ac.jp.

Alteration in genes which takes place during malignant conversion and progression could be potential targets for gene therapy. We previously identified REIC/Dkk-3 as a gene whose expression is reduced in many human cancers. Here, we showed that expression of REIC/Dkk-3 was consistently reduced in human prostate cancer tissues in a stage-dependent manner. Forced expression of REIC/Dkk-3 induced apoptosis in human prostate cancer cell lines lacking endogenous REIC/Dkk-3 expression but not in REIC/Dkk-3-proficient normal prostate epithelial and stromal cells. The apoptosis involved c-Jun-NH₂-kinase activation, mitochondrial translocation of Bax, and reduction of Bcl-2. A single injection of an adenovirus vector carrying REIC/Dkk-3 showed a dramatic antitumor effect on a xenotransplanted human prostate cancer. Thus, REIC/Dkk-3 could be a novel target for gene-based therapy of prostate cancer.

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