Please use this identifier to cite or link to this item:
Title: Context-Specific Regulation of NF-κB Target Gene Expression by EZH2 in Breast Cancers
Authors: Lee, S.T.
Li, Z.
Wu, Z.
Aau, M.
Guan, P.
Karuturi, R.K.M.
Liou, Y.C. 
Yu, Q. 
Issue Date: 2-Sep-2011
Citation: Lee, S.T., Li, Z., Wu, Z., Aau, M., Guan, P., Karuturi, R.K.M., Liou, Y.C., Yu, Q. (2011-09-02). Context-Specific Regulation of NF-κB Target Gene Expression by EZH2 in Breast Cancers. Molecular Cell 43 (5) : 798-810. ScholarBank@NUS Repository.
Abstract: Both EZH2 and NF-κB contribute to aggressive breast cancer, yet whether the two oncogenic factors have functional crosstalk in breast cancer is unknown. Here, we uncover an unexpected role of EZH2 in conferring the constitutive activation of NF-κB target gene expression in ER-negative basal-like breast cancer cells. This function of EZH2 is independent of its histone methyltransferase activity but requires the physical interaction with RelA/RelB to promote the expression of NF-κB targets. Intriguingly, EZH2 acts oppositely in ER-positive luminal-like breast cancer cells and represses NF-κB target gene expression by interacting with ER and directing repressive histone methylation on their promoters. Thus, EZH2 functions as a double-facet molecule in breast cancers, either as a transcriptional activator or repressor of NF-κB targets, depending on the cellular context. These findings reveal an additional mechanism by which EZH2 promotes breast cancer progression and underscore the need for developing context-specific strategy for therapeutic targeting of EZH2 in breast cancers. © 2011 Elsevier Inc.
Source Title: Molecular Cell
ISSN: 10972765
DOI: 10.1016/j.molcel.2011.08.011
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Jun 30, 2022


checked on Jun 30, 2022

Page view(s)

checked on Jun 23, 2022

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.