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MCF7 cells acquire estrogen-independent proliferation after long-term estrogen deprivation (LTED), which recapitulates endocrine therapy resistance. LTED cells can become primed for apoptosis, but the underlying mechanism is largely unknown. We previously reported that  Eleanor  non-coding RNAs (ncRNAs) upregulate the  ESR1  gene in LTED cells. Here, we show that  Eleanors  delineate the topologically associating domain (TAD) of the  ESR1  locus in the active nuclear compartment of LTED cells. The TAD interacts with another transcriptionally active TAD, which is 42.9 Mb away from  ESR1  and contains a gene encoding the apoptotic transcription factor FOXO3. Inhibition of a promoter-associated  Eleanor  suppresses all genes inside the  Eleanor  TAD and the long-range interaction between the two TADs, but keeps  FOXO3  active to facilitate apoptosis in LTED cells. These data indicate a role of ncRNAs in chromatin domain regulation, which may underlie the apoptosis-prone nature of therapy-resistant breast cancer cells and could be good therapeutic targets.

The Eleanor ncRNAs activate the topological domain of the ESR1 locus to balance against apoptosis