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Transcriptional profiling of 22Rv1 cells upon treatments of RBN-2397 and tapinarof

ABSTRACT: Transcriptional profiling of 22Rv1 cells upon treatments of RBN-2397 and tapinarof

PROVIDER: PRJNA1122860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29366046_1.fastq.gz	Fastqsanger.gz
	SRR29366046_2.fastq.gz	Fastqsanger.gz
	SRR29366047_1.fastq.gz	Fastqsanger.gz
	SRR29366047_2.fastq.gz	Fastqsanger.gz
	SRR29366048_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of 22Rv1 cells upon treatments of RBN-2397 and tapinarof

Project description:Small molecule inhibitors of the mono (ADP) ribosyl transferase PARP7 are being evaluated therapeutically as a monotherapy for tumors overexpressing PARP7 and in combination with immune checkpoint inhibitors. We previously showed that sensitivity to the PARP7 inhibitor (PARP7i) RBN-2397 could be enhanced by co-treatment with agonists of the aryl hydrocarbon receptor (AHRa) in cell lines that show strong intrinsic sensitivity to RBN-2397. Here we demonstrate that a range of tumor cell lines that are relatively insensitive to PARP7i or AHRa as individual agents are profoundly sensitive to the combination. Our data show that this synergistic response is dependent on AHR/ARNT and is associated with increased levels of nuclear AHR and increased transcription of AHR target genes. In some hormone-dependent cell lines, we find that combination treatment is associated with proteasomal turnover of the steroid hormone receptors, androgen receptor (AR) and estrogen receptor (ER). Both wildtype and therapy-resistant mutant forms of these receptors are degraded upon treatment with AHRa and PARP7i in breast and prostate cancer models. These results suggest that combining PARP7i with AHRa may extend the utility of these drugs to a wider range of tumors, including those that are refractory to hormone therapy.

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