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Defective prostate cancer motility in two transgenic mouse models of kallikrein-3 deficiency.
Transgenic mouse models for prostate cancerogenesis will contribute to the evaluation of their relevance as targets for chemoprevention. The protease kallikrein-3 (KLK3) is considered to be an important factor involved in prostate cancer development. Overexpression of KLK3 has been described to enhance androgen-independent prostate cancer cell growth and migration. However, a causal role for KLK3 in the development of prostate cancer remains to be evaluated. Previously, we have generated transgenic mice with tissue-specific expression of KLK3 in the prostate. Here, we provide a comprehensive analysis of the prostate architecture and morphological changes in KLK3 transgenic animals. In contrast to mice expressing a wild-type KLK3, KLK3 transgenic animals revealed a significantly altered prostate gland, which included partial loss of the luminal epithelium. In addition, KLK3 transgenic animals had a markedly disturbed smooth muscle layer. Furthermore, the prostate of KLK3 transgenic animals showed a pronounced reduction of the androgen receptor (AR) target genes prostate-specific antigen (PSA) and keratin 18 (K18), without showing major changes in the expression of androgen-induced genes, as determined by quantitative RT-PCR. In addition, KLK3 transgenic mice showed impaired spontaneous cell migration and invasiveness in a wound-healing assay. All of these results point to an essential role of KLK3 in prostate development and in prostate cancer progression. Therefore, KLK3 transgenic mice may be considered to be valuable tools to study the contribution of KLK3 to prostate cancer development. to that of the non-degenerate case. The second case corresponds to a $\pi$-distributed initial energy gap and the figure shows the occupation of the eigenstates under influence of the coherent coupling. We remark that the coherent coupling does not affect the spectrum itself. It only shifts

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