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Genome-wide maps of chromatin state in patient-derived model (PDX) of AR-positive or negative CRPC

ABSTRACT: Genome-wide maps of chromatin state in patient-derived model (PDX) of AR-positive or negative CRPC

PROVIDER: PRJNA794723 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17442933.fastq.gz	Fastqsanger.gz
	SRR17442934.fastq.gz	Fastqsanger.gz
	SRR17442935.fastq.gz	Fastqsanger.gz
	SRR17442936.fastq.gz	Fastqsanger.gz
	SRR17442937.fastq.gz	Fastqsanger.gz

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Genome-wide maps of chromatin state in patient-derived model (PDX) of AR-positive or negative CRPC

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BET inhibitor Pelabresib and AR inhibitor enzalutamide perturbed pathways in prostate cancer CRPC PDX LuCaP 35CR

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Project description:Castration-resistant PCa (CRPC) remains androgen receptor (AR) dependent. There are multiple mechanisms for reactivation of AR including expression of the constitutively active AR splice variant, AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR without unique targets. We have used an LN95 cell line that endogenously expresses AR and a low level of AR-V7 to compare the activities of the isoforms and to determine whether there is differential regulation of target genes. The transcriptomes for AR and AR-V7 were identified using RNA-Seq.

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BET inhibitor Pelabresib and AR inhibitor enzalutamide perturbed pathways in prostate cancer CRPC PDX LuCaP 35CR

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BET inhibitor Pelabresib and AR inhibitor enzalutamide perturbed pathways in prostate cancer CRPC PDX LuCaP 77CR

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AR signalling in castration resistant prostate cancer (CRPC)

Project description:AR signalling in castration resistant prostate cancer (CRPC)

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Androgen Receptor splice variant V7 (AR-V7) mediates AR signalling in castration resistant prostate cancer (CRPC) [ChIP-exo]

Project description:CRPC remains AR dependent. There are multiple mechanisms for reactivation of AR including expression of constitutively active AR splices variant AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR. We have used an LNCaP cell line that expresses AR-V7 in response to doxycycline to compare DNA interactions of the two isoforms and to identify differential regulation of target genes. ChIP-exo method was used to map AR and AR-V7 interaction with DNA in LNCaP engineered cell line (LNCaP AR-V7) at single base resolution.

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Project description:In castration-resistant prostate cancer (CRPC), clinical response to androgen receptor (AR) antagonists is limited mainly due to AR-variants expression and restored AR signaling. The metabolite spermine is most abundant in prostate and it decreases as prostate cancer progresses, but its functions remain poorly understood. Here, we show spermine inhibits full-length androgen receptor (AR-FL) and androgen receptor splice variant 7 (AR-V7) signaling and suppresses CRPC cell proliferation by directly binding and inhibiting protein arginine methyltransferase PRMT1. Spermine reduces H4R3me2a modification at the AR locus and suppresses AR binding as well as H3K27ac modification levels at AR target genes. Spermine supplementation restrains CRPC growth in vivo. PRMT1 inhibition also suppresses AR-FL and AR-V7 signaling and reduces CRPC growth. Collectively, we demonstrate spermine as an anticancer metabolite by inhibiting PRMT1 to transcriptionally inhibit AR-FL and AR-V7 signaling in CRPC, and we indicate spermine and PRMT1 inhibition as powerful strategies overcoming limitations of current AR-based therapies in CRPC.

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