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Abstract

Volume 15, Issue 5 (September 2013) 15, 584–585; doi: 10.1038/aja.2013.64

SPDEF: a molecular switch for E-cadherin expression that promotes prostate cancer metastasis

Mary Osisami and Evan T Keller

Department of Urology, University of Michigan, Ann Arbor, MI 48105, USA

Correspondence: Dr ET Keller, (etkeller@umich.edu)

27 May 2013

Abstract

In order to design effective therapies for prostate cancer, a clear understanding of mechanisms that contribute to various components of prostate cancer progression is necessary. Study of metastasis suppressor genes, i.e., genes that can inhibit metastasis, is an important field of study that can lead to identification of therapeutic targets to diminish metastasis. E-cadherin has been implicated as an important inhibitor of metastasis. Thus, understanding how it is regulated may lead towards defining mechanism of metastasis suppressor activity. Through a series of studies using genetically-modified cells, Pal et al. determined that SAM Pointed Domain ETS transcription Factor (SPDEF) serves as a molecular switch to turn on E-cadherin expression and thus regulate tumor aggressiveness. They determined SPDEF achieved regulation of expression through binding to and regulating the SPDEF promoter. These findings provide a strong rationale to explore targeting SPDEF for inhibition of prostate cancer metastasis.

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Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.