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Status |
Public on Oct 01, 2015 |
Title |
LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer [ChIP-Seq] |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
Summary |
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.
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Overall design |
ChIP-Seq examination of ER binding sites in MCF7 cells.
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Contributor(s) |
Yu J, Xue X |
Citation(s) |
26364613 |
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Submission date |
Jul 23, 2015 |
Last update date |
May 15, 2019 |
Contact name |
Jindan Yu |
E-mail(s) |
jindan.yu@emory.edu
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Organization name |
Emory University
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Department |
Urology
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Lab |
Jindan Yu's lab
|
Street address |
E330, 1760 Haygood Dr NE
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City |
Atlanta |
State/province |
GA |
ZIP/Postal code |
30322 |
Country |
USA |
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Platforms (1) |
GPL15456 |
Illumina HiScanSQ (Homo sapiens) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE71298 |
LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer |
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Relations |
BioProject |
PRJNA290780 |
SRA |
SRP061461 |