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Sci. STKE, 14 June 2005
Vol. 2005, Issue 288, p. pe27
[DOI: 10.1126/stke.2882005pe27]


Crossroads of Estrogen Receptor and NF-{kappa}B Signaling

Debajit K. Biswas*, Sindhu Singh, Qian Shi, Arthur B. Pardee, and J. Dirk Iglehart

Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Surgery, Brigham and Women’s Hospital, Boston, MA 02115, USA.

Abstract: Cellular homeostasis in higher organisms is maintained by balancing cell growth, differentiation, and death. Two important systems that transmit extracellular signals into the machinery of the cell nucleus are the signaling pathways that activate nuclear factor {kappa}B (NF-{kappa}B) and estrogen receptor (ER). These two transcription factors induce expression of genes that control cell fates, including proliferation and cell death (apoptosis). However, ER has anti-inflammatory effects, whereas activated NF-{kappa}B initiates and maintains cellular inflammatory responses. Recent investigations elucidated a nonclassical and nongenomic effect of ER: inhibition of NF-{kappa}B activation and the inflammatory response. In breast cancer, antiestrogen therapy might cause reactivation of NF-{kappa}B, potentially rerouting a proliferative signal to breast cancer cells and contributing to hormone resistance. Thus, ER ligands that selectively block NF-{kappa}B activation could provide specific potential therapy for hormone-resistant ER-positive breast cancers.

*Corresponding author. E-mail: Debajit_Biswas{at}

Citation: D. K. Biswas, S. Singh, Q. Shi, A. B. Pardee, J. D. Iglehart, Crossroads of Estrogen Receptor and NF-{kappa}B Signaling. Sci. STKE 2005, pe27 (2005).

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