Journal
NATURE COMMUNICATIONS
Volume 10, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-09320-9
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Funding
- NIH [R01GM114142, U54CA217297, R01GM129338, P50CA186784]
- ACS Institutional Research Grant [14-196-01]
- Breast Cancer Research Foundation (BCRF) [16-142, 17-143, 18-145]
- DOD [W81XWH-14-1-0326]
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Recent studies have demonstrated that chromatin architecture is linked to the progression of cancers. However, the roles of 3D structure and its dynamics in hormone-dependent breast cancer and endocrine resistance are largely unknown. Here we report the dynamics of 3D chromatin structure across a time course of estradiol (E2) stimulation in human estrogen receptor a (ER alpha)-positive breast cancer cells. We identified subsets of temporally highly dynamic compartments predominantly associated with active open chromatin and found that these highly dynamic compartments showed higher alteration in tamoxifenresistant breast cancer cells. Remarkably, these compartments are characterized by active chromatin states, and enhanced ER alpha binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. We finally identified a set of ER alpha-bound promoter-enhancer looping genes enclosed within altered domains that are enriched with cancer invasion, aggressiveness or metabolism signaling pathways. This large-scale analysis expands our understanding of high-order temporal chromatin reorganization underlying hormonedependent breast cancer.
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