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This process involves the activation and recruitment of WNT signalling components, which compensate for the loss of BRD4 and drive resistance in various cancer models.

Dynamic chromatin immunoprecipitation sequencing and self-transcribing active regulatory region sequencing of enhancer profiles reveal that BET-resistant states are characterized by remodelled regulatory landscapes, involving the activation of a focal MYC enhancer that recruits WNT machinery in response to BET inhibition.

Next, we investigated whether the rebound of BRD4 targets is associated with changes in the enhancer landscape. To probe regulatory pathways involved in the re-expression of Brd4 targets, we analyzed the transcriptomes of sensitive and resistant cells generated using three independent PRC2 sh RNAs ().

Under long-term JQ1 treatment, resistant cells showed a global loss of enhancer-associated H3K27ac marks, which was reversible upon drug withdrawal (Extended Data Fig. Almost half of the genes associated with upregulated pathways harbor H3K27me3 marks in sensitive cells (Extended Data Fig.

Four sh RNAs showed an outstanding enrichment that was consistent between replicates, despite almost five weeks of independent culture (The finding that suppression of Suz12, a component of the PRC2 complex, promotes resistance to JQ1 was surprising in two ways.

First, a recent report, based on studies in nerve sheath tumors, has implicated Suz12 deficiency as a condition that sensitizes to BET inhibition).

Similarly, while BET inhibition triggers acute MYC repression in human leukaemias regardless of their sensitivity, resistant leukaemias are uniformly characterized by their ability to rapidly restore MYC transcription.

To this end, we determined the JQ1 sensitivity in 246 human cell lines (Extended Data Fig.

5a), and selected 3 sensitive and 3 resistant lines from 3 cancer subtypes for dynamic transcriptional profiling.

To identify factors involved in primary and acquired BET resistance in leukemia, we performed a chromatin-focused RNAi screen in a sensitive MLL/AF9; Nras -driven AML model, and investigated dynamic transcriptional profiles in sensitive and resistant murine and human leukemias.

Our screen reveals that suppression of the PRC2 complex, contrary to effects in other contexts, promotes BET inhibitor resistance in AML.

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