한빛사 논문
Abstract
Yun-Yong Park1,†, Kyounghyun Kim2,†, Sang-Bae Kim1, Bryan T. Hennessy1,2, Soo Mi Kim1, Eun Sung Park1, Jae Yun Lim1, Jane Li1,3, Yiling Lu1, Ana Maria Gonzalez-Angulo1,4, Woojin Jeong1,5, Gordon B. Mills1, Stephen Safe2,6, Ju-Seog Lee1,*
1Department of Systems Biology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
2Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA
3Gynecologic Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
4Breast Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
5Department of Life Science, Division of Life and Pharmaceutical Sciences, Center for Cell Signaling and Drug Discovery Research, Ewha Woman's University, Seoul, Korea
6Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX, USA
*Correspondence: Ju-Seog Lee
Abstract
ESR1 is one of the most important transcription factors and therapeutic targets in breast cancer. By applying systems-level re-analysis of publicly available gene expression data, we uncovered a potential regulator of ESR1. We demonstrated that orphan nuclear receptor NR2E3 regulates ESR1 via direct binding to the ESR1 promoter with concomitant recruitment of PIAS3 to the promoter in breast cancer cells, and is essential for physiological cellular activity of ESR1 in estrogen receptor (ER)-positive breast cancer cells. Moreover, expression of NR2E3 was significantly associated with recurrence-free survival and a favourable response to tamoxifen treatment in women with ER-positive breast cancer. Our results provide mechanistic insights on the regulation of ESR1 by NR2E3 and the clinical relevance of NR2E3 in breast cancer.
Keywords:breast cancer;genomics;microarray;NR2E3;nuclear receptor
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