LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer [ChIP-Seq]. Homo sapiens

HOTAIR is up-regulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or tamoxifen treatment. Overall design: ChIP-Seq examination of ER binding sites in MCF7 cells.