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Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [RNAseq]

ABSTRACT: Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [RNAseq]

PROVIDER: PRJNA1069376 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27732939.fastq.gz	Fastqsanger.gz
	SRR27732940.fastq.gz	Fastqsanger.gz
	SRR27732941.fastq.gz	Fastqsanger.gz
	SRR27732942.fastq.gz	Fastqsanger.gz
	SRR27732943.fastq.gz	Fastqsanger.gz

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Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [Quantseq]

Project description:Hepatocellular carcinoma (HCC) emerges from chronic inflammation to which activation of hepatic stellate cells (HSCs) contributes by shaping a pro-tumorigenic microenvironment. Key to this process is p62, whose inactivation leads to enhanced hepatocarcinogenesis. Here, we show that while p62 positively regulates STING ubiquitination by TRIM32 by displacing NBR1, which results in the activation of the interferon (IFN) cascade, NBR1 prevents TRIM32 interaction with and the activation of STING, leading to impaired IFN synthesis. NBR1 also antagonizes STING function by promoting its trafficking from the Golgi to the endosome-lysosomal degradative cascade independent of autophagy. Importantly, NBR1 deletion completely reverts the tumor-promoting function of p62-deficient HSCs. The upregulation of the STING-IFN pathway by NBR1 deficiency enhances the anti-tumor response mediated by CD8+ T cells. These results identify NBR1 as a synthetic vulnerability of p62-deficiency in HSCs. NBR1 loss, by promoting the STING/IFN pathway, boosts anti-tumor CD8+ T cell responses to restrain HCC.

2024-10-22 | GSE254277 | GEO

Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [RNAseq]

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Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [Quantseq]

Project description:Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma [Quantseq]

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Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma.

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p62/SQSTM1 by binding to vitamin D receptor inhibits hepatic stellate cell activity, fibrosis and liver cancer

Project description:Hepatic stellate cells (HSC) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC). Vitamin D receptor (VDR) activation in HSC inhibits liver inflammation and fibrosis. Here we show that p62/SQSTM1, a protein that is upregulated in liver parenchymal cells but downregulated in HCC-associated HSC, negatively regulates HSC activation. Total body or HSC-specific p62 ablation potentiates HSC activation and enhances inflammation, fibrosis and HCC progression. We demonstrate that p62 directly interacts with VDR and RXR promoting their heterodimerization, which is critical for VDR:RXR target genes recruitment. Loss of p62 in HSC impairs the repression of fibrosis and inflammation by VDR agonists. This demonstrates that p62 is a negative regulator of liver inflammation and fibrosis through its ability to promote VDR signaling in HSC, whose activation supports HCC development.

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