alexa Adenovirus-mediated overexpression of REIC Dkk-3 selectively induces apoptosis in human prostate cancer cells through activation of c-Jun-NH2-kinase.


Journal of Cancer Science & Therapy

Author(s): Abarzua F, Sakaguchi M, Takaishi M, Nasu Y, Kurose K,

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Abstract 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. This article was published in Cancer Res and referenced in Journal of Cancer Science & Therapy

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