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Epigenetics of Estrogen Receptor Signaling: Role in Hormonal Cancer Progression and Therapy
Department of Cellular and Structural Biology, UTHSCSA, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
Department of Obstetrics and Gynecology, UTHSCSA, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
* Author to whom correspondence should be addressed.
Received: 4 January 2011; in revised form: 11 March 2011 / Accepted: 25 March 2011 / Published: 29 March 2011
Abstract: Estrogen receptor (ERa) signaling plays a key role in hormonal cancer progression. ERa is a ligand-dependent transcription factor that modulates gene transcription via recruitment to the target gene chromatin. Emerging evidence suggests that ERa signaling has the potential to contribute to epigenetic changes. Estrogen stimulation is shown to induce several histone modifications at the ERα target gene promoters including acetylation, phosphorylation and methylation via dynamic interactions with histone modifying enzymes. Deregulation of enzymes involved in the ERa-mediated epigenetic pathway could play a vital role in ERa driven neoplastic processes. Unlike genetic alterations, epigenetic changes are reversible, and hence offer novel therapeutic opportunities to reverse ERa driven epigenetic changes. In this review, we summarize current knowledge on mechanisms by which ERa signaling potentiates epigenetic changes in cancer cells via histone modifications.
Keywords: estrogen receptor; histone modifications; epigenetics; breast cancer; hormonal cancers
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Cite This Article
MDPI and ACS Style
Mann, M.; Cortez, V.; Vadlamudi, R.K. Epigenetics of Estrogen Receptor Signaling: Role in Hormonal Cancer Progression and Therapy. Cancers 2011, 3, 1691-1707.
Mann M, Cortez V, Vadlamudi RK. Epigenetics of Estrogen Receptor Signaling: Role in Hormonal Cancer Progression and Therapy. Cancers. 2011; 3(2):1691-1707.
Mann, Monica; Cortez, Valerie; Vadlamudi, Ratna K. 2011. "Epigenetics of Estrogen Receptor Signaling: Role in Hormonal Cancer Progression and Therapy." Cancers 3, no. 2: 1691-1707.