Down regulation of PSA by C/EBPα is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell Line
DSpace/Manakin Repository
Down regulation of PSA by C/EBPα is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell Line
| Title: | Down regulation of PSA by C/EBPα is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell Line |
| Author: |
Glass, Jonathan; Yin, Hong; Radomska, Hanna S.; Tenen, Daniel Geoffrey
Note: Order does not necessarily reflect citation order of authors. |
| Citation: | Yin, Hong, Hanna S. Radomska, Daniel G. Tenen, and Jonathan Glass. 2006. Down regulation of PSA by C/EBPα is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell Line. BMC Cancer 6: 158. |
| Full Text & Related Files: |
1544346.pdf (612.5Kb; PDF) 
|
| Abstract: | Background: C/EBPα is a transcription factor essential for terminal differentiation of several cell types. It has not known if C/EBPα protein is expressed and functions in the prostate gland. Methods: The presence of C/EBPα in normal and cancerous prostate epithelium was examined by immunochemistry. Over expression of C/EBPα in LNCaP cells was conducted with retrovirus-mediated transduction. PSA expression was examined by RT-PCR and western blot and PSA promoter activity by luciferase reporter assay. Results: In normal prostate C/EBPα was expressed in the basal layer of the epithelium. In prostate cancer C/EBPα was detected at low levels throughout the cancers and in advanced prostate cancer C/EBPα expression was associated with decreased expression of AR and PSA. Overexpression of C/EBPα inhibited epigenetically PSA expression and was accompanied by the loss of expression of AR. Transient increase of C/EBPα inhibited the PSA promoter/enhancer activity independently of expression of AR. Conclusion: In LNCaP cells C/EBPα over expression inhibits expression of PSA by AR -dependent and independent mechanisms and by extinguishing AR expression provides a model for hormonal independent cell growth. |
| Published Version: | doi:10.1186/1471-2407-6-158 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1544346/pdf/ |
| Terms of Use: | This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA |
| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:4874840 |
| Downloads of this work: |
This item appears in the following Collection(s)
-
HMS Scholarly Articles [16253]
Contact administrator regarding this item (to report mistakes or request changes)
