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Abarzua, F. et al.

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

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.[1]

References

Adenovirus-mediated overexpression of REIC/Dkk-3 selectively induces apoptosis in human prostate cancer cells through activation of c-Jun-NH2-kinase. Abarzua, F., Sakaguchi, M., Takaishi, M., Nasu, Y., Kurose, K., Ebara, S., Miyazaki, M., Namba, M., Kumon, H., Huh, N.H. Cancer Res. (2005) [Pubmed]

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