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Transcriptomic profiles of CT26 syngeneic tumor tissues following treatment with the dual EP2/EP4 antagonist TP-18.

ABSTRACT: Transcriptomic profiles of CT26 syngeneic tumor tissues following treatment with the dual EP2/EP4 antagonist TP-18.

PROVIDER: PRJNA1254115 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33247794_1.fastq.gz	Fastqsanger.gz
	SRR33247794_2.fastq.gz	Fastqsanger.gz
	SRR33247796_1.fastq.gz	Fastqsanger.gz
	SRR33247796_2.fastq.gz	Fastqsanger.gz
	SRR33247798_1.fastq.gz	Fastqsanger.gz

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Transcriptomic profiles of CT26 syngeneic tumor tissues following treatment with the dual EP2/EP4 antagonist TP-18.

Project description:To investigate the antitumor mechanisms of the dual EP2/EP4 antagonist TP-18, we conducted RNA-seq-based transcriptomic analysis of CT26 tumors, with or without TP-18 treatment.

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Gene expression profiles in CT26 syngeneic tumor tissues after EP4 antagonist TP-16(BY001), anti-PD-1 antibody or combination treatment

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Gene expression profiles in CT26 syngeneic tumor tissues after EP4 antagonist TP-16(BY001), anti-PD-1 antibody or combination treatment

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Project description:The discovery of immune checkpoint inhibitor (ICI) has highlighted the clinical importance of immune evasion in cancer. However, only a fraction of cancer patients show response to ICI, raising a question on immune suppression mechanisms other than immune checkpoint. In this study, we examined the role of the lipid inflammatory mediator PGE2 in immune evasion of the ICI-insensitive Lewis Lung Carcinoma line 1 (LLC1) mouse model. Inhibition of PGE receptors, EP2 and EP4, significantly suppressed tumor growth through the modulation of host immune cells. Single cell RNA-sequencing analysis revealed that EP2/4 inhibition elicited anti-tumor immunity through the reprogramming of inflammatory myeloid cells by downregulating expression of genes in NFB signaling and actions and suppression of the mregDC-regulatory T cell axis by downregulating genes associated with regulatory T cell recruitment and activation. Taken together, our work suggests that PGE2-EP2/EP4 signaling induces proinflammatory myeloid and tolerogenic lymphoid environments in ICI-insensitive tumors, which is amenable to EP2 and EP4 inhibitors..

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