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

Mohamed Osama Ali Abdalla, Tatsuro Yamamoto, Kazumitsu Maehara, Jumpei Nogami, Yasuyuki Ohkawa, Hisashi Miura, Rawin Poonperm, Ichiro Hiratani, Hideki Nakayama, Mitsuyoshi Nakao () and Noriko Saitoh ()
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Mohamed Osama Ali Abdalla: Kumamoto University
Tatsuro Yamamoto: Kumamoto University
Kazumitsu Maehara: Kyushu University
Jumpei Nogami: Kyushu University
Yasuyuki Ohkawa: Kyushu University
Hisashi Miura: RIKEN Center for Biosystems Dynamics Research (BDR)
Rawin Poonperm: RIKEN Center for Biosystems Dynamics Research (BDR)
Ichiro Hiratani: RIKEN Center for Biosystems Dynamics Research (BDR)
Hideki Nakayama: Kumamoto University
Mitsuyoshi Nakao: Kumamoto University
Noriko Saitoh: Kumamoto University

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract 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.

Date: 2019
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DOI: 10.1038/s41467-019-11378-4

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