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Sublethal necroptosis signaling promotes inflammation and liver cancer

ABSTRACT: Sublethal necroptosis signaling promotes inflammation and liver cancer

PROVIDER: PRJNA702161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13724000_1.fastq.gz	Fastqsanger.gz
	SRR13724000_2.fastq.gz	Fastqsanger.gz
	SRR13724001_1.fastq.gz	Fastqsanger.gz
	SRR13724001_2.fastq.gz	Fastqsanger.gz
	SRR13724002_1.fastq.gz	Fastqsanger.gz

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Sublethal necroptosis signaling promotes inflammation and liver cancer

Project description:We developed a genetic mouse model of chronic necroptosis activation in hepatocytes (in the presence of basal NF-kB activity) that lead to hepatocellular carcinoma. Blocking Necroptosis (RIP3) or NF-kB-(IKKβ) activation in those mice blocked hepatocarcinogenesis.

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Quantitative analysis of phosphoproteome in necroptosis reveals a role of TRIM28 phosphorylation in promoting necroptosis-induced cytokine production

Project description:Necroptosis is a form of regulated necrotic cell death which promotes inflammation. In cells undergoing necroptosis, the activated RIPK1 kinase mediates the formation of RIPK1/RIPK3/MLKL complex to promote MLKL oligomerization and execution of necroptosis. RIPK1 kinase activity also promotes cell-autonomous activation of proinflammatory cytokine production in necroptosis. However, the signaling pathways downstream of RIPK1 kinase in necroptosis and how RIPK1 kinase activation controls inflammatory response induced by necroptosis are still largely unknown. Here we quantitatively measured the temporal dynamics of over 7000 confident phosphosites during necroptosis using mass spectrometry. Our study defined a RIPK1-dependent phosphorylation pattern in late necroptosis that is associated with a proinflammatory component marked by p-S473 TRIM28. We show that the activation of p38 MAPK mediated by oligomerized MLKL promotes the phosphorylation of S473 TRIM28, which in turn mediates inflammation during late necroptosis. Taken together, our study illustrates a mechanism by which p38 MAPK may be activated by oligomerized MLKL to promote inflammation in necroptosis.

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The Role of Necroptosis-mediated Inflammation in Hepatocellular Carcinoma

Project description:Non-alcoholic hepatosteatosis (NASH) due to metabolic syndrome or diabetes mellitus has been identified as the fastest growing cause of hepatocellular carcinoma (HCC), the fourth leading cause of cancer related deaths in the world. Therapeutic options for HCC are limited, and survival after diagnosis is poor (>10%). Thus, a better understanding of the mechanisms that drive the progression of NASH to HCC is critical in developing new strategies to prevent/treat HCC. Chronic inflammation is a key player in the pathogenesis of HCC, however, pathways that drive chronic hepatic inflammation in NASH-driven HCC is not known. Necroptosis is a regulated mode of cell death that causes inflammation and is activated in the livers of patients with NASH. Therefore, we tested whether necroptosis-mediated inflammation plays a role in the progression of NASH to HCC in a mouse model of NASH-induced HCC.

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Project description:The Role of Necroptosis-mediated Inflammation in Hepatocellular Carcinoma

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SETDB1 safeguards genome stability against necroptosis and bowel inflammation (ChIP-seq)

Project description:The aetiology of bowel inflammatory disease (IBD) is a multifactorial interplay between heredity and environment1-3. Here we report SETDB1, a histone methyltransferase (HMTs) for histone H3 lysine 9 trimethylation (H3K9me3) whose deficiency participates in the pathogenesis of IBD. We found that SETDB1 level decreased in IBD patients and that mice with reduced SETDB1 in intestinal stem cells (ISCs) developed spontaneous terminal ileitis and colitis. SETDB1 safeguards genome stability4, of which the loss in ISCs released repression of endogenous retrovirus (ERVs), the retrovirus-like elements with long repeats that comprise ~8% of genome5. Excessive viral mimicry generated by motivated ERVs triggered Z-DNA-binding protein 1 (ZBP1) dependent necroptosis, which irreversibly disrupted the homeostasis of epithelial barrier and promoted bowel inflammation. Of note, genome instability, reactive ERVs, upregulation of ZBP1 and necroptosis were seen in IBD patients. Pharmaceutic inhibition of RIP3 showed curative effect in SETDB1 deficient mice, suggesting therapy targeting ISC necroptosis may represent a new approach for severe IBD treatment.

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Setdb1 safeguards genome stability against stem cell necroptosis and bowel inflammation (RNA-seq)

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