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Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ChIP-Seq]

ABSTRACT: Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ChIP-Seq]

PROVIDER: PRJNA720142 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14159830_1.fastq.gz	Fastqsanger.gz
	SRR14159830_2.fastq.gz	Fastqsanger.gz
	SRR14159831_1.fastq.gz	Fastqsanger.gz
	SRR14159831_2.fastq.gz	Fastqsanger.gz
	SRR14159832_1.fastq.gz	Fastqsanger.gz

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Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer

Project description:Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer

| PRJNA720138 | ENA

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [HiChIP-Seq]

Project description:This study profiles chromatin accessibility, gene expresison, transcription factor binding, and three-dimensional DNA-DNA contact changes upon rapid SWI/SNF ATPase inactivation in prostate cancer cells. SWI/SNF ATPases activity was disabled using a novel PROTAC degrader compound targeting the SMARCA2, SMARCA4 and PBRM1 subunits of the SWI/SNF remodeling complex.

2021-10-28 | GSE171591 | GEO

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ChIP-Seq]

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Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ATAC-Seq]

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Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [RNA-Seq]

2021-10-28 | GSE171523 | GEO

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [RNA-Seq]

Project description:Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [RNA-Seq]

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Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ATAC-Seq]

Project description:Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ATAC-Seq]

| PRJNA720136 | ENA

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [HiChIP-Seq]

Project description:Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [HiChIP-Seq]

| PRJNA720143 | ENA

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer.

Project description:The switch/sucrose non-fermentable (SWI/SNF) complex has a crucial role in chromatin remodelling1 and is altered in over 20% of cancers2,3. Here we developed a proteolysis-targeting chimera (PROTAC) degrader of the SWI/SNF ATPase subunits, SMARCA2 and SMARCA4, called AU-15330. Androgen receptor (AR)+ forkhead box A1 (FOXA1)+ prostate cancer cells are exquisitely sensitive to dual SMARCA2 and SMARCA4 degradation relative to normal and other cancer cell lines. SWI/SNF ATPase degradation rapidly compacts cis-regulatory elements bound by transcription factors that drive prostate cancer cell proliferation, namely AR, FOXA1, ERG and MYC, which dislodges them from chromatin, disables their core enhancer circuitry, and abolishes the downstream oncogenic gene programs. SWI/SNF ATPase degradation also disrupts super-enhancer and promoter looping interactions that wire supra-physiologic expression of the AR, FOXA1 and MYC oncogenes themselves. AU-15330 induces potent inhibition of tumour growth in xenograft models of prostate cancer and synergizes with the AR antagonist enzalutamide, even inducing disease remission in castration-resistant prostate cancer (CRPC) models without toxicity. Thus, impeding SWI/SNF-mediated enhancer accessibility represents a promising therapeutic approach for enhancer-addicted cancers.

| S-EPMC8770127 | biostudies-literature

Targeting SWI/SNF ATPases reduces cell invasiveness and plasticity in core transcription factors-addicted neuroblastoma

Project description:Neuroblastoma (NB) comprises mesenchymal (MES) and adrenergic (ADRN) subtypes, and the cell identity is determined by core transcription factors (TFs). However, the binding mechanism of these TFs to DNA and the epigenetic mechanisms governing NB plasticity remain unclear. In this study, we investigated the impact of targeting SWI/SNF ATPases with SMARCA2/4 dual degraders on NB cells. Our results revealed that depletion of SWI/SNF ATPases compacted cis-regulatory elements, diminished enhancer activity, and displaced core TFs (MYCN, HAND2, PHOX2B, and GATA3) from DNA, suppressing transcriptional programs linked to plasticity and invasiveness. These findings underscore the pivotal role of SWI/SNF ATPases in driving NB progression, positioning them as promising therapeutic targets.

2024-08-28 | GSE240724 | GEO

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