Using this model, we studied the gene expression profile during prostate carcinogenesis using a cDNA array method. The results were confirmed by RT-PCR, western blotting, and immunohistochemical (IHC) analyses. Seventeen genes were differentially expressed, and three of them with the highest level of overexpression were selected for further analysis. They included: Testosterone-repressed prostatic message-2 (TRPM-2), matrix metalloproteinase-7, (MMP-7), and inhibitor ofdifferentiation or DNA binding (Id-1) (6). Increased expression of TRPM-2 and MMP-7 was observed in both pre- and malignant samples after sex hormone treatment, indicating their role in the early stages of hormone response and PCA development. In contrast, Id-1 was expressed at relatively low levels in all pre- malignant samples, but its level of expression increased in malignant cells, suggesting its potential role as a PCA biomarker. More significantly, we found that the level of Id-1 expression was higher in poorly differentiatedlesions than in well-differentiated carcinomas (Figure 1), suggesting that the levels of Id-1 expression may be correlated with tumor malignancy (6).
Hyperplasia (4M LP)
Dysplasia (12M LP)
Figure 1. IMH study of Id-1 protein expression. Sections from normal LPs, hyperplasia, dysplasia, and carcinoma regions were stained with specific Id-1 antibodies. Note absent to weak Id-1 expression detected in normal LPs and in non-malignant lesions, while PCA cells exhibit high Id-1 immunoreactivity (400 x).
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