File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cdc25B as a Steroid Receptor Coactivator

TitleCdc25B as a Steroid Receptor Coactivator
Authors
Issue Date2004
Citation
Vitamins And Hormones, 2004, v. 68, p. 231-256 How to Cite?
AbstractThe traditional role of the Cdc25 family of dual-specificity phosphatases is to activate cyclin-dependent kinases (CDKs) to enable progression through the cell cycle. This chapter reports that in addition to its cell cycle role, Cdc25B functions as a novel steroid receptor coactivator (SRC). When overexpressed in transgenic mammary glands, Cdc25B can up-regulate the expression of two estrogen receptor (ER)-target genes: cyclin D1 and Lactoferrin. In addition, when coexpressed with ER, Cdc25B can coactivate an ER-dependent reporter in the presence of estradiol. The coactivation of Cdc25B can be extended to the glucocorticoid receptor (GR), progesterone receptor (PR), and androgen receptor (AR). Because of the respective importance of ER and AR in breast and prostate cancer, this chapter focuses on the coactivation of both receptors by Cdc25B. We demonstrate that Cdc25B can interact directly with these nuclear receptors, recruit and enhance the activity of histone acetyltransferases (HATs), and potentiate cell-free transcription independent of its cell cycle regulatory function. Furthermore, because Cdc25B is up-regulated in highgrade and poorly differentiated prostate tumors, which are likely transiting from the hormone-dependent to hormone-independent state, we hypothesize that the coactivation of AR by Cdc25B may induce genes responsible for this progression. Taken together, it is highly conceivable that Cdc25B can promote neoplasia by its two disparate functions of (1) coactivation to induce higher levels of expression of steroid receptor target genes and (2) its role of activating CDKs to deregulate progression of the cell cycle, DNA replication, and mitosis. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/120763
ISSN
2015 Impact Factor: 2.161
2015 SCImago Journal Rankings: 1.103

 

DC FieldValueLanguage
dc.contributor.authorChua, SSen_HK
dc.contributor.authorMa, Zen_HK
dc.contributor.authorNgan, Een_HK
dc.contributor.authorTsai, SYen_HK
dc.date.accessioned2010-09-26T09:55:11Z-
dc.date.available2010-09-26T09:55:11Z-
dc.date.issued2004en_HK
dc.identifier.citationVitamins And Hormones, 2004, v. 68, p. 231-256en_HK
dc.identifier.issn0083-6729en_HK
dc.identifier.urihttp://hdl.handle.net/10722/120763-
dc.description.abstractThe traditional role of the Cdc25 family of dual-specificity phosphatases is to activate cyclin-dependent kinases (CDKs) to enable progression through the cell cycle. This chapter reports that in addition to its cell cycle role, Cdc25B functions as a novel steroid receptor coactivator (SRC). When overexpressed in transgenic mammary glands, Cdc25B can up-regulate the expression of two estrogen receptor (ER)-target genes: cyclin D1 and Lactoferrin. In addition, when coexpressed with ER, Cdc25B can coactivate an ER-dependent reporter in the presence of estradiol. The coactivation of Cdc25B can be extended to the glucocorticoid receptor (GR), progesterone receptor (PR), and androgen receptor (AR). Because of the respective importance of ER and AR in breast and prostate cancer, this chapter focuses on the coactivation of both receptors by Cdc25B. We demonstrate that Cdc25B can interact directly with these nuclear receptors, recruit and enhance the activity of histone acetyltransferases (HATs), and potentiate cell-free transcription independent of its cell cycle regulatory function. Furthermore, because Cdc25B is up-regulated in highgrade and poorly differentiated prostate tumors, which are likely transiting from the hormone-dependent to hormone-independent state, we hypothesize that the coactivation of AR by Cdc25B may induce genes responsible for this progression. Taken together, it is highly conceivable that Cdc25B can promote neoplasia by its two disparate functions of (1) coactivation to induce higher levels of expression of steroid receptor target genes and (2) its role of activating CDKs to deregulate progression of the cell cycle, DNA replication, and mitosis. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.relation.ispartofVitamins and Hormonesen_HK
dc.titleCdc25B as a Steroid Receptor Coactivatoren_HK
dc.typeArticleen_HK
dc.identifier.emailNgan, E: engan@hkucc.hku.hken_HK
dc.identifier.authorityNgan, E=rp00422en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0083-6729(04)68008-3en_HK
dc.identifier.scopuseid_2-s2.0-3242886010en_HK
dc.identifier.hkuros100263en_HK
dc.identifier.volume68en_HK
dc.identifier.spage231en_HK
dc.identifier.epage256en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChua, SS=7201550437en_HK
dc.identifier.scopusauthoridMa, Z=7403600106en_HK
dc.identifier.scopusauthoridNgan, E=22234827500en_HK
dc.identifier.scopusauthoridTsai, SY=7403478781en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats