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GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (ChIP-Seq)

ABSTRACT: GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (ChIP-Seq)

PROVIDER: PRJNA1049035 | ENA |

REPOSITORIES: ENA

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GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer

Project description:GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer

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Project description:GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (RNA-Seq)

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GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (RNA-Seq)

Project description:Darolutamide is the latest FDA-approved antiandrogen for the treatment of metastatic prostate cancer. Despite its efficacy in prolonging disease-free survival, drug resistance invariably develops. This study aims to understand the molecular mechanisms underlying darolutamide resistance and identify potential therapeutic targets for overcoming the resistance.

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GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (ChIP-Seq)

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GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [RNA-seq]

Project description:The androgen receptor (AR) antagonist darolutamide has very recently been approved for the treatment of non-metastatic castration resistant prostate cancer (PCa). Here we determined the genome-wide effects of darolutamide on cis-acting regulatory elements involved in androgen signaling with a focus on enhancer and super-enhancer (SE) regions. Darolutamide strongly depleted the AR from regulatory elements and abolished the AR transcriptional signaling. Using two different androgen-dependent PCa cell lines we identified genomic-regions with different affinities for the AR in androgen-stimulated, androgen-depleted and darolutamide-antagonized conditions. Altogether, our findings demonstrate that darolutamide is a potent AR antagonist blocking genome-wide AR signaling and AR enhancer activation. Further, we show a dynamic AR cistrome and concomitant adapting chromatin environment to varying conditions and identified regions with high AR affinity in cell lines and tissue samples.

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [ChIP-seq]

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TET2 lesions enhance the aggressiveness of CEBPA-mutant AML by rebalancing GATA2 expression [WGBS]

Project description:The myeloid transcription factor CEBPA is recurrently biallelically mutated (i.e., double mutated; CEBPADM) in acute myeloid leukemia (AML) with a combination of hypermorphic N-terminal mutations (CEBPANT), promoting expression of the leukemia-associated p30 isoform, and amorphic C-terminal mutations. CEBPADM AML features recurrent co-occurring mutations including GATA2 lesions, however insights into mechanisms governing this co-mutational spectrum are incomplete. By combining transcriptomic and epigenomic analyses of CEBPA-TET2 co-mutated patients with models thereof, we identify GATA2 as a conserved target of the CEBPA-TET2 mutational axis, providing a rationale for the mutational spectra in CEBPADM AML. Mechanistically, we suggest that elevated CEBPA levels, driven by CEBPANT, mediate recruitment of TET2 to the Gata2 distal hematopoietic enhancer thereby increasing Gata2 expression. Conversely, CEBPADM AML gains a competitive advantage through TET2 loss, by decreasing Gata2 promoter demethylation thereby rebalancing GATA2 levels. Of clinical relevance, demethylating treatment of Cebpa-Tet2 co-mutated AML restores Gata2 levels and prolongs disease latency.

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