The polycomb group protein EZH2 is involved in progression of prostate cancer

Sooryanarayana Varambally, Saravana M. Dhanasekaran, Ming Zhou, Terrence R. Barrette, Chandan Kumar-Sinha, Martin G. Sanda, Debashis Ghosh, Kenneth J. Pienta, Richard G. A. B. Sewalt, Arie P. Otte, Mark A. Rubin and Arul M. Chinnaiyan ()
Additional contact information
Sooryanarayana Varambally: University of Michigan Medical School
Saravana M. Dhanasekaran: University of Michigan Medical School
Ming Zhou: University of Michigan Medical School
Terrence R. Barrette: University of Michigan Medical School
Chandan Kumar-Sinha: University of Michigan Medical School
Martin G. Sanda: University of Michigan Medical School
Debashis Ghosh: University of Michigan Medical School
Kenneth J. Pienta: University of Michigan Medical School
Richard G. A. B. Sewalt: University of Amsterdam
Arie P. Otte: University of Amsterdam
Mark A. Rubin: University of Michigan Medical School
Arul M. Chinnaiyan: University of Michigan Medical School

Nature, 2002, vol. 419, issue 6907, 624-629

Abstract: Abstract Prostate cancer is a leading cause of cancer-related death in males and is second only to lung cancer. Although effective surgical and radiation treatments exist for clinically localized prostate cancer, metastatic prostate cancer remains essentially incurable. Here we show, through gene expression profiling1, that the polycomb group protein enhancer of zeste homolog 2 (EZH2)2,3 is overexpressed in hormone-refractory, metastatic prostate cancer. Small interfering RNA (siRNA) duplexes4 targeted against EZH2 reduce the amounts of EZH2 protein present in prostate cells and also inhibit cell proliferation in vitro. Ectopic expression of EZH2 in prostate cells induces transcriptional repression of a specific cohort of genes. Gene silencing mediated by EZH2 requires the SET domain and is attenuated by inhibiting histone deacetylase activity. Amounts of both EZH2 messenger RNA and EZH2 protein are increased in metastatic prostate cancer; in addition, clinically localized prostate cancers that express higher concentrations of EZH2 show a poorer prognosis. Thus, dysregulated expression of EZH2 may be involved in the progression of prostate cancer, as well as being a marker that distinguishes indolent prostate cancer from those at risk of lethal progression.

Date: 2002
References: Add references at CitEc
Citations: View citations in EconPapers (9)

Downloads: (external link)
https://www.nature.com/articles/nature01075 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:419:y:2002:i:6907:d:10.1038_nature01075

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature01075

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().