Characterization of an ICII82, 780-Induced, Estrogen Receptor (ER)-beta Mediated Apoptotic Pathway in Prostate Cancer Cells and Establishment of (ER)-beta-Regulated Electrophile-Processing Phase II Enzyme Downregulation as a Promotional Factor in Human Prostatic Carcinogenesis
Abstract
To investigate the role of ER-beta in human prostate carcinogenesis, and in growth regulation of a prostate cancer cell line (DU145), we proposed: 1) to study effects of antiestrogens/estrogens on growth of DU145 cells, 2) to Immunostain tissue sections from discarded human radical prostatectomy specimens and to perform semiquantitative RT-PCR on microdissected tissues to determine the level of ER-beta expression in normal and abnormal prostate tissues. Under Specific Aim 1, the proposed works have been completed and the results had been published in Cancer Research Journal and reported in the first progress report. In addition, we demonstrated the antiestrogen-induced cell growth inhibition in DU145 cells might be due to the induction of cell cycle arrest at GO-GI phase. Under Specific Aim 2, Using G017 we showed that in normal prostates, ER-beta was strongly expressed in the nuclei of basal epithelial cells. ER-beta expression was transiently elevated in early PIN lesions, but progressively diminished in higher grade PIN lesions. Similarly, ER-beta immunostaining was markedly diminished in Gleason grade 3 and 4 adenocarcinomas and absent in higher-grade cancers. ER-beta expression reappeared in metastatic prostatic carcinomas. The results were also compared to ER-alpha and androgen receptor expressions in those samples.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2001
- Accession Number
- ADA398092
Entities
People
- Shuk-mei Ho
Organizations
- University of Massachusetts Medical School