Abstract
Background: How glucocorticoids affect ER-positive breast cancer cell proliferation is unclear. Results: GR occupies ERα-binding regions (EBRs) via tethering to AP1 and ERα. Conclusion: Interaction of GR with EBRs via ERα and AP1 inhibits E2-ERα activity. Significance: Breast tumors with ERα and AP1 expression will be responsive to glucocorticoid therapy; the study establishes a foundation for personalized medicine for BC. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.
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CITATION STYLE
Karmakar, S., Jin, Y., & Nagaich, A. K. (2013). Interaction of glucocorticoid receptor (GR) with estrogen receptor (ER) α and activator protein 1 (AP1) in dexamethasone-mediated interference of ERα activity. Journal of Biological Chemistry, 288(33), 24020–24034. https://doi.org/10.1074/jbc.M113.473819
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