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Expression profile of 22Rv1 cells with GFP or HNF4G exogenous expression when treated with BETi ABBV-075

ABSTRACT: Expression profile of 22Rv1 cells with GFP or HNF4G exogenous expression when treated with BETi ABBV-075

PROVIDER: PRJNA1071591 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27812155_1.fastq.gz	Fastqsanger.gz
	SRR27812155_2.fastq.gz	Fastqsanger.gz
	SRR27812156_1.fastq.gz	Fastqsanger.gz
	SRR27812156_2.fastq.gz	Fastqsanger.gz
	SRR27812157_1.fastq.gz	Fastqsanger.gz

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Expression profile of 22Rv1 cells with GFP or HNF4G exogenous expression when treated with BETi ABBV-075

Project description:To study the consequence of HNF4G target genes expression with ABBV-075 treatment in cells that have BETi-independent HNF4G expression, we performed RNA-Seq on 22Rv1 cells that exogenously express HNF4G using GFP expression as control.

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Identification of potential ABBV-075 responsive markers in mouse skin

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Identification of potential ABBV-075 responsive markers in human PBMCs

Project description:To identify genes that are modulated by BET inhibitors in blood, we determined global gene expression changes in ABBV-075-treated human PBMC samples

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Identification of potential ABBV-075 responsive markers in mouse whole blood

Project description:To identify genes that are modulated by BET inhibitors in blood, we determined global gene expression changes in ABBV-075-treated mouse whole blood samples

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BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

Project description:BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

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HNF4G, AR, FOXA1, H3K4me1, H3K27acetyl binding sites upon knockdown and overexpression of HNF4G in 22Rv1 and LNCaP prostate cancer cells respectively

Project description:HNF4G is a gastrointestinal tissue enriched master transcriptional regulator seen overexpressed in a subset of prostate cancer. Here we have mapped binding sites of HNF4G, AR, Foxa1, H3K4me1, H3K27acetyl upon knockdown and overexpression of HNF4G in in 22Rv1 and LNCaP cells respectively

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BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

Project description:BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

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BET inhibitor ABBV-075 perturbed pathways in prostate cancer organoid MSK-PCa17

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MYC family amplification dictates sensitivity to BET bromodomain protein inhibitor Mivebresib (ABBV-075) in small cell lung cancer

Project description:Small-cell lung cancer (SCLC) accounts for nearly 15% of all lung cancers. Although patients respond to first line therapy readily, rapid relapse is inevitable with few treatment options in the second line setting. Here, we describe SCLC cell lines harboring amplification of MYC and MYCN, but not MYCL1 nor non-amplified MYC cell lines, exhibit superior sensitivity to treatment with the pan-BET bromodomain protein inhibitor Mivebresib (ABBV-075). Silencing MYC and MYCN partially rescued SCLC cell lines harboring these respective amplifications from the anti-proliferative effects of mivebresib. Furthermore, the activity of mivebresib in SCLC cell lines occurs primarily through BRD2, rather than BRD4. Further characterization of genome-wide binding of MYC, MYCN, and MYCL1 uncovered unique enhancer and epigenetic preferences. Our study suggests that chromatin landscapes could establish cell states with unique gene expression programs, conveying sensitivity to epigenetic inhibitors such as mivebresib.

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Contribution of BET proteins to androgen (DHT)-stimulated gene expression program

Project description:Competitive inhibitors of acetyl-lysine binding to the bromodomains of the BET (bromodomain and extra terminal) family are being developed for the treatment of solid and heme malignancies. BET family member BRD4 function at enhancers/super-enhancers has been shown to sustain signal-dependent or pathogenic gene expression programs. Here we tested the hypothesis that the transcription factor drivers of castration-resistant prostate cancer (CRPC) clinical progression, including the Androgen Receptor (AR), are critically dependent on BRD4 and thus represent a sensitive solid tumor indication for the BET inhibitor ABBV-075. DHT-stimulated transcription of AR target genes was inhibited by ABBV-075 without significant effect on AR protein expression. Further, ABBV-075 disrupted DHT-stimulated recruitment of BET family member BRD4 to gene regulatory regions co-occupied by AR, including the well-established PSA and TMPRSS2 enhancers. Persistent BET inhibition disrupted the composition and function of AR occupied enhancers as measured by a reduction in AR and H3K27Ac ChIP signal and inhibition of eRNA transcription. ABBV-075 displayed potent anti-proliferative activity in multiple models of resistance to second generation anti-androgens and inhibited the activity of AR-V7 and the AR LBD gain-of-function mutations, F877L and L702H. ABBV-075 was also a potent inhibitor of MYC and the TMPRSS2-ETS fusion protein, important parallel transcription factor drivers of CRPC.

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