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Combination of EZH2 inhibitor and STING agonist in melanoma cell lines

ABSTRACT: Combination of EZH2 inhibitor and STING agonist in melanoma cell lines

PROVIDER: PRJNA719921 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14148700_1.fastq.gz	Fastqsanger.gz
	SRR14148700_2.fastq.gz	Fastqsanger.gz
	SRR14148701_1.fastq.gz	Fastqsanger.gz
	SRR14148701_2.fastq.gz	Fastqsanger.gz
	SRR14148702_1.fastq.gz	Fastqsanger.gz

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Combination of EZH2 inhibitor and STING agonist in melanoma cell lines

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Transcriptome-wide identification of STING agonist programed B cells

Project description:We employed RNA-seq to study the transcriptomic change in B lymphocytes in response to STING agonist. Transcriptomic analysis of wild type and TMEM173–/– B cells stimulated with STING agonist revealed that the inflammatory response pathway enriched in 3'3'-cGAMP treated WT B cells but lacking in Tmem173-/-B cells comprised of a cluster containing inhibitory regulators, provoking STING signal to evade immune surveillance by inducing an immunosuppressive B cell population.

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EZH2 Inhibition Activates a dsRNA-STING-Interferon Stress Mechanism that Potentiates Response to PD-1 Check-Point Blockade in Prostate Cancer

Project description:Prostate cancers are considered immunologically ‘cold’ tumors given the very few patients who respond to checkpoint inhibitor therapy (CPI). Recently, enrichment of interferon stimulated genes (ISGs) predicts a favorable response to CPI across various disease sites. The enhancer of zeste homolog-2 (EZH2) is over-expressed in prostate cancer and is known to negatively regulate ISGs. Here, we demonstrate that a majority of ISGs are not directly silenced by EZH2 mediated H3K27me3 deposition, but instead in a poised chromatin state associated with accessible chromatin (ATAC+) and H3K27ac deposition. Inhibition of EZH2 catalytic activity in prostate cancer models activates a dsRNA-STING-ISG cellular stress response upregulating genes involved in antigen presentation, Th-1 chemokine signaling, and interferon (IFN) response, including PD-L1 that is dependent on STING activation. EZH2 inhibition combined with PD-1 CPI significantly enhances anti-tumor response dependent on up-regulation of tumor PD-L1 expression. Further, combination therapy significantly increases intratumoral trafficking of activated CD8+ T-cells and M1 tumor associated macrophages (TAMs) with concurrent loss of M2 TAMs. Our study identifies EZH2 as a potent inhibitor of antitumor immunity and responsiveness to CPI. This data suggests EZH2 inhibition is a novel therapeutic direction to enhance prostate cancer response to PD-1 CPI.

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STING agonist alters the transcriptional profiles of HSPCs in melanoma-bearing mouse model

Project description:STING agonist alters the transcriptional profiles of HSPCs in melanoma-bearing mouse model

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