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BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity [RNA-Seq]

ABSTRACT: BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity [RNA-Seq]

PROVIDER: PRJNA765320 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16010365.fastq.gz	Fastqsanger.gz
	SRR16010366.fastq.gz	Fastqsanger.gz
	SRR16010367.fastq.gz	Fastqsanger.gz
	SRR16010368.fastq.gz	Fastqsanger.gz
	SRR16010369.fastq.gz	Fastqsanger.gz

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Project description:Targeting chromatin binding proteins and modifying enzymes can concomitantly affect tumor cell proliferation and survival, as well as enhance anti-tumor immunity and augment cancer immunotherapies. By screening a small molecule library of epigenetics-based therapeutics, BET bromodomain inhibitors (BETi) were identified as agents that sensitize tumor cells to the anti-tumor activity of CD8+ T-cells. BETi modulated tumor cells to be sensitized to the cytotoxic effects of the pro-inflammatory cytokine TNF. By preventing the recruitment of BRD4 to p65-bound cis-regulatory elements, BETi suppressed the induction of inflammatory gene expression, including the key NF-B target genes BIRC2 (cIAP1) and BIRC3 (cIAP2). Disruption of pro-survival NF-B signaling by BETi led to unrestrained TNF-mediated activation of the extrinsic apoptotic cascade and tumor cell death. Administration of BETi in combination with T-cell bispecific (TCB) antibodies increased bystander killing of tumor cells and enhanced tumor growth inhibition in vivo in a TNF-dependent manner. This novel epigenetic mechanism of immunomodulation may guide future use of BETi as adjuvants for immune oncology agents.

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BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity [ChIP-Seq, ATAC-Seq]

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BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity

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Epigenetic priming enhances anti-tumor immunity in resistant ovarian cancer

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CTLA-4 tail fusion enhances CAR-T anti-tumor immunity

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Cyclin-dependent kinase 9 is a therapeutic target for anti-TNF resistant inflammatory bowel disease

Project description:The treatment of auto-inflammatory diseases is often limited by resistance to single cytokine blockade, primarily anti-TNF antibodies. This is a particularly important cause of treatment failure in inflammatory bowel disease (IBD). The transcription factor T-bet is a critical regulator of intestinal homeostasis and is genetically linked to mucosal inflammation by causal variation in its binding sites. However, transcription factors such as T-bet are difficult to target therapeutically. Using CDK9 inhibitors, we show that modulation of P-TEFb (cyclinT1/CDK9), a transcriptional elongation factor downstream of T-bet, potently represses genes responsible for pro-inflammatory signalling, and in particular genes regulated by T-bet. Remarkably, CDK9 inhibition targets genes that are highly expressed in anti-TNF resistant IBD and that predict non-response to anti-TNF therapy. Collectively, our findings reveal CDK9 as a potential target in anti-TNF resistant IBD, which has the potential for rapid translation to the clinic.

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