Over Expression of ID-1 in Prostate Cancer.

摘要

PURPOSE: The helix-loop-helix protein Id-1 serves to prevent basic helix-loop-helix transcription factors from binding to DNA, thus, inhibiting the transcription of differentiation associated genes. Over expression of Id-1 has been reported in certain tumors, such as breast, esophageal, pancreatic and medullary thyroid cancers. In Noble rats we have previously demonstrated that up-regulation of Id-1 is closely associated with the development of sex hormone induced prostate cancers. Therefore, we hypothesized that over expression of Id-1 would also occur in human prostate cancer and Id-1 protein may serve as a potential marker for prostate carcinogenesis. To test this hypothesis we analyzed Id-1 messenger RNA and protein expression by in situ hybridization and immunohistochemical study in human normal prostate, benign prostatic hyperplasia (BPH) and prostate cancer tissues. MATERIALS AND METHODS: Pathological specimens were obtained from 19 patients with BPH and 47 with prostate carcinoma, representing a complete range of Gleason grades. A total of 12 normal prostate tissue specimens were used for comparison. Immunohistochemical study was performed using the polyclonal antibody against human Id-1 protein and an RNA probe was generated from Id-1 complementary DNA for in situ hybridization. RESULTS: Negative to weak expression of Id-1 in normal prostate or BPH tissue was observed on immunohistochemical study and in situ hybridization. In contrast, all prostate cancer biopsies showed significant positive Id-1 expression in tumor cells at the messenger RNA and protein levels. Furthermore, Id-1 expression was stronger in poorly differentiated than in well differentiated carcinomas, suggesting that the level of Id-1 expression may be associated with tumor malignancy. CONCLUSIONS: Our results suggest that over expression of Id-1 may have important roles in the development of prostate cancer. The potential use of Id-1 protein as a marker for prostate cancer should be further explored.