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FBP1 loss disrupts liver metabolism and results in distinct transcriptome

ABSTRACT: FBP1 loss disrupts liver metabolism and results in distinct transcriptome

PROVIDER: PRJNA559465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9937440_1.fastq.gz	Fastqsanger.gz
	SRR9937440_2.fastq.gz	Fastqsanger.gz
	SRR9937431_1.fastq.gz	Fastqsanger.gz
	SRR9937431_2.fastq.gz	Fastqsanger.gz
	SRR9937432_1.fastq.gz	Fastqsanger.gz

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FBP1 loss disrupts liver metabolism and results in distinct transcriptome

Project description:This study set out to globally compare the liver transcriptomes from 24-week old wild type (WT) and FBP1-deficient mice. Total RNA was isolated from 10 snap frozen liver tissue samples using RNeasy Mini Kit (Qiagen). 250~300 bp insert eukaryotic mRNA derived cDNA non-directional libraryRNA libraries were prepared using standard Illumina protocols. The sequencing were performed on Illumina Platform PE150, with 20M raw reads/sample.

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FBP1 loss disrupts liver metabolism and promotes tumourigenesis through a hepatic stellate cell senescence secretome

Project description:Crosstalk between deregulated hepatocyte metabolism and cells within the tumour microenvironment, and consequent effects on liver tumourigenesis, are incompletely understood. We show here that hepatocyte specific loss of the gluconeogenic enzyme fructose 1,6-bisphosphatase 1 (FBP1) disrupts liver metabolic homeostasis and promotes tumour progression. FBP1 is universally silenced in both human and murine liver tumours, and hepatocyte-specific Fbp1 deletion results in steatosis, concomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phenotype (SASP). Depleting senescent HSCs by senolytic treatment with dasatinib/quercetin or ABT-263 inhibits tumour progression. We further demonstrate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; blocking its release with the small molecule inflachromene limits FBP1-dependent HSC activation, subsequent SASP development, and tumour progression. Collectively, these findings provide genetic evidence for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical link between hepatocyte metabolism and HSC senescence that promotes tumour growth.

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An EZH2-FBP1 Feedback Circuitry Promotes Tumorigenesis in Gluconeogenic Tissues

Project description:We report that enhancer of zeste homologue 2 (EZH2) represses the expression of a rate-limiting gluconeogenic enzyme fructose-1, 6 -bisphosphatase 1 (FBP1) to promote tumorigenesis. More intriguingly, FBP1 inhibits EZH2 methyltransferase activity by binding EZH2 at targeted loci and dissembles the polycomb complex, which constitutes a negative feedback loop for EZH2-initiated signalings. We performed ChIP-Seq assays using the EZH2 and H3K27me3 antibody in HCC cells with vector control, FBP1 wild-type (WT) or FBP1 S169A re-expression. FBP1 WT severely reduced EZH2 and H3K27me3 signals. Conversely, FBP1 S169A exhibits much less effects on global or target-specific H3K27me3. In addition, ChIP-Seq assays with the FBP1 uncover a significant overlap between EZH2 and FBP1 binding sites, confirming that FBP1 inhibits EZH2 though physical interactions in the vicinity of chromosomes. Collectively, these studies reveal an unexpected crosstalk between metabolic and epigenetic events, and identify a new mechanistic circuitry highlighting EZH2 inhibitors as liver and kidney cancer therapeutics.

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FBP1 loss disrupts liver metabolism and promotes tumorigenesis through a hepatic stellate cell senescence secretome.

Project description:The crosstalk between deregulated hepatocyte metabolism and cells within the tumour microenvironment, as well as the consequent effects on liver tumorigenesis, are not completely understood. We show here that hepatocyte-specific loss of the gluconeogenic enzyme fructose 1,6-bisphosphatase 1 (FBP1) disrupts liver metabolic homeostasis and promotes tumour progression. FBP1 is universally silenced in both human and murine liver tumours. Hepatocyte-specific Fbp1 deletion results in steatosis, concomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phenotype. Depleting senescent HSCs by 'senolytic' treatment with dasatinib/quercetin or ABT-263 inhibits tumour progression. We further demonstrate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; blocking its release with the small molecule inflachromene limits FBP1-dependent HSC activation, the subsequent development of the senescence-associated secretory phenotype and tumour progression. Collectively, these findings provide genetic evidence for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical crosstalk between hepatocyte metabolism and HSC senescence that promotes tumour growth.

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