The role of 14-3-3 beta in transcriptional activation of estrogen receptor alpha and its involvement in proliferation of breast cancer cells
- Authors
- Kim, Yoonseo; Kim, Hyungjin; Jang, Sung-Wuk; Ko, Jesang
- Issue Date
- 14-10월-2011
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Breast cancer; Estrogen receptor; 14-3-3
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.414, no.1, pp.199 - 204
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 414
- Number
- 1
- Start Page
- 199
- End Page
- 204
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/111375
- DOI
- 10.1016/j.bbrc.2011.09.056
- ISSN
- 0006-291X
- Abstract
- The estrogen receptor (ER) functions as a transcription factor that mediates the effects of estrogen. ER alpha, which plays a crucial role in the development and progression of breast cancer, is activated by estrogen binding, leading to receptor phosphorylation, dimerization, and recruitment of co-activators and chaperons to the estrogen-bound receptor complex. The 14-3-3 proteins bind to target proteins via phosphorylation and influence many cellular events by altering their subcellular localization or acting as a chaperone. However, regulation of ER alpha expression and transactivation by the 14-3-3 proteins has not been reported. We demonstrate that 14-3-3 beta functions as a positive regulator of ER alpha through a direct protein-protein interaction in an estrogen-dependent manner. Ectopic expression of 14-3-3 beta stimulated ER alpha-mediated transcriptional activity in MCF-7 breast cancer cells. Enhanced ER alpha transcriptional activity due to 14-3-3 beta increased the expressions of the endogenous ER alpha target genes, leading to proliferation of breast cancer cells. We suggest that 14-3-3 beta has oncogenic potential in breast cancer via binding to ER alpha and activation of the transcriptional activity of ER alpha. (C) 2011 Elsevier Inc. All rights reserved.
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