Home  |  Archive  |  Online Submission  |  News & Events  |  Subscribe  |  APFA  |  Society  |  Links  |  Contact Us  |  中文版
Search   
 
Journal

Ahead of print
Authors' Accepted
    Manuscripts
new!
Current Issue
Archive
Acknowledgments
Special Issues
Browse by Category

Manuscript Submission

Online Submission
Online Review
Instruction for Authors
Instruction for Reviewers
English Corner new!

About AJA

About AJA
Editorial Board
Contact Us
News

Resources & Services

Advertisement
Subscription
Email alert
Proceedings
Reprints

Download area

Copyright licence
EndNote style file
Manuscript word template
Guidance for AJA figures
    preparation (in English)

Guidance for AJA figures
    preparation (in Chinese)

Proof-reading for the
    authors

AJA Club (in English)
AJA Club (in Chinese)

Links

Meetings
Journals
Societies & Institutes
Hospitals
Databases & Libraries
Companies
Websites
Other links

 
Abstract

Volume 14, Issue 3 (May 2012) 14, 436–450; 10.1038/aja.2011.160

Specific changes in the expression of imprinted genes in prostate cancer--implications for cancer progression and epigenetic regulation

Teodora Ribarska, Klaus-Marius Bastian, Annemarie Koch and Wolfgang A Schulz

Department of Urology, Heinrich Heine University, Düsseldorf, Germany

Correspondence: Professor WA Schulz, (wolfgang.schulz@uni-duesseldorf.de)

Received 8 October 2011; Revised 7 November 2011; Accepted 1 December 2011; Advance online publication 27 February 2012

Abstract

Epigenetic dysregulation comprising DNA hypermethylation and hypomethylation, enhancer of zeste homologue 2 (EZH2) overexpression and altered patterns of histone modifications is associated with the progression of prostate cancer. DNA methylation, EZH2 and histone modifications also ensure the parental-specific monoallelic expression of at least 62 imprinted genes. Although it is therefore tempting to speculate that epigenetic dysregulation may extend to imprinted genes, expression changes in cancerous prostates are only well documented for insulin-like growth factor 2 (IGF2). A literature and database survey on imprinted genes in prostate cancer suggests that the expression of most imprinted genes remains unchanged despite global disturbances in epigenetic mechanisms. Instead, selective genetic and epigenetic changes appear to lead to the inactivation of a sub-network of imprinted genes, which might function in the prostate to limit cell growth induced via the PI3K/Akt pathway, modulate androgen responses and regulate differentiation. Whereas dysregulation of IGF2 may constitute an early change in prostate carcinogenesis, inactivation of this imprinted gene network is rather associated with cancer progression.

Keywords: androgen signalling; imprinted genes; loss of imprinting; PI3K signalling; prostate cancer

PDF | 中文摘要 |

 
Browse:  2817
 
Copyright 1999-2017  Shanghai Materia Medica, Shanghai Jiao Tong University.  All rights reserved