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MC38/gp100 cells after type I PRMT inhibitor treatment

ABSTRACT: MC38/gp100 cells after type I PRMT inhibitor treatment

PROVIDER: PRJNA679810 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13092382_1.fastq.gz	Fastqsanger.gz
	SRR13092382_2.fastq.gz	Fastqsanger.gz
	SRR13092383_1.fastq.gz	Fastqsanger.gz
	SRR13092383_2.fastq.gz	Fastqsanger.gz
	SRR13092384_1.fastq.gz	Fastqsanger.gz

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Chromatin accessibility in MC38/gp100 cells after type I PRMT inhibitor treatment

Project description:Chromatin accessibility in MC38/gp100 cells after type I PRMT inhibitor treatment

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Differential expression genes analysis in MC38/gp100 cell line with DMSO or type I PRMT inhibitor treatment

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Chromatin accessibility in MC38/gp100 cells after type I PRMT inhibitor treatment

Project description:Immunotherapies have produced dramatic responses in reducing tumor growth and prolonging overall survival to unprecedented rates in melanoma, lung cancer, renal cancer and mismatch repair deficient colon cancer patients. Despite approvals for immune checkpoint inhibitors in a wide range of cancers, the majority of patients’ relapse following initial response to immunotherapy or fail to respond altogether. These failures can be attributed to an insufficient immune response against tumors and/or mechanisms co-opted by tumor cells to produce a suppressive tumor microenvironment. Therefore, identification of combination strategies to enhance the response rates of immunotherapies to a broader patient population are the current subject of intensive basic and clinical research. Type I PRMTs have been described as regulators of immune response pathways in several cell types by direct arginine methylation on specific substrates, as well as through indirect mechanisms. Recent work has suggested that arginine methylation may have a role in tumor immunity, yet these roles remain poorly understood. Using the skin cutaneous melanoma (SKCM) TCGA dataset, we show that increased expression of Type I PRMTs is associated with poor clinical response and decreased immune infiltration in melanoma patients. Through a series of preclinical tumor models, we demonstrate that inhibition of Type I PRMTs can increase hallmarks of an inflamed tumor microenvironment and sensitivity to inhibition of the PD-(L)1 signaling axis. Accordingly, Type I PRMT inhibition synergizes with immune checkpoint blockade to induce durable and effective antitumor responses in an array of immunocompetent tumor models. These data provide a rationale to combine Type I PRMT inhibitors with checkpoint blockade to maximize clinical benefit in cancer patients.

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MC38/gp100 cells after type I PRMT inhibitor treatment

Project description:This SuperSeries is composed of the SubSeries listed below.

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Tumor intrinsic PRMT5 inhibition through MTAP loss predicts response to the first-in-class type I PRMT inhibitor, GSK3368715

Project description:Type I Protein Arginine Methyltransferases (PRMTs) catalyze asymmetric dimethylation of arginine (ADMA) residues on numerous protein substrates to modulate their activity. Type I PRMTs and many of their substrates have been implicated in human cancers, suggesting that inhibiting Type I PRMT activity offers a tractable approach for therapeutic intervention. The current report describes GSK3368715 (EPZ019997), a potent, reversible Type I PRMT inhibitor with anti-tumor activity against human cancer cells both in vitro and in vivo. GSK3368715 reduces ADMA on numerous substrates and concomitantly increases monomethyl (MMA) and symmetric dimethyl arginine (SDMA) levels. Inhibition of PRMT5, the major type II PRMT, attenuates this induction and produces synergistic antiproliferative effects in combination with GSK3368715 in cancer cells. PRMT5 activity is inhibited by 2-methylthioadenosine (MTA), a naturally occurring metabolite that accumulates in tumor cells deficient for the enzyme Methylthioadenosine Phosphorylase (MTAP). MTAP deletion in cancer cell lines correlates with sensitivity to GSK3368715, indicating a sufficient degree of PRMT5 inhibition from MTA accumulation to achieve a tumor cell-intrinsic combination. These data provide the rationale to explore MTAP status as a biomarker strategy for patient selection to maximize the anti-tumor activity of GSK3368715.

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