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A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity

ABSTRACT: A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity

PROVIDER: PRJNA603281 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10969430.fastq.gz	Fastqsanger.gz
	SRR10969431.fastq.gz	Fastqsanger.gz
	SRR10969432.fastq.gz	Fastqsanger.gz
	SRR10969433.fastq.gz	Fastqsanger.gz
	SRR10969434.fastq.gz	Fastqsanger.gz

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A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity.

Project description:During the cancerous transformation of normal hepatocytes into hepatocellular carcinoma (HCC), the enzyme catalyzing the first rate-limiting step of glycolysis, namely the glucokinase (GCK), is replaced by the higher affinity isoenzyme, hexokinase 2 (HK2). Here, we show that in HCC tumors the highest expression level of HK2 is inversely correlated to GCK expression, and is associated to poor prognosis for patient survival. To further explore functional consequences of the GCK-to-HK2 isoenzyme switch occurring during carcinogenesis, HK2 was knocked-out in the HCC cell line Huh7 and replaced by GCK, to generate the Huh7-GCK+/HK2- cell line. HK2 knockdown and GCK expression rewired central carbon metabolism, stimulated mitochondrial respiration and restored essential metabolic functions of normal hepatocytes such as lipogenesis, VLDL secretion, glycogen storage. It also reactivated innate immune responses and sensitivity to natural killer cells, showing that consequences of the HK switch extend beyond metabolic reprogramming.

| S-EPMC7886870 | biostudies-literature

A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity

Project description:HK2 is expressed in the hepatocellular carcinoma cell line Huh7 while GCK is expressed in the normal hepatocyte. In order to analyze the functional consequences of the expression of one or other of the hexokinases (HK2 or GCK) we have invalidated the expression of HK2 and induced the expression of GCK in Huh7 cells. We analyzed transcriptome of both cell line

2021-01-15 | GSE144214 | GEO

Hepatitis C Virus Infection Activates a Novel Innate Pathway Involving IKKα in Lipogenesis and Viral Assembly

Project description:Hepatitis C virus interacts extensively with host factors not only to establish productive infection but also to trigger unique pathological processes. Our recent genome-wide siRNA screen demonstrated that IKKα is a critical host factor for HCV. Here we describe a novel NF-κB-independent and kinase-mediated nuclear function of IKKα in HCV assembly. HCV infection, through its 3’-untranslated region, interacts with DDX3X to activate IKKα, which translocates to the nucleus and induces a CBP/p300-mediated transcriptional program involving SREBPs. This novel innate pathway induces lipogenic genes and enhances core-associated lipid droplet formation to facilitate viral assembly. Chemical inhibitors of IKKα suppress HCV infection and IKKα-induced lipogenesis, offering a proof-of-concept approach for novel HCV therapeutic development. Our results show that HCV commands a novel mechanism to its advantage by exploiting intrinsic innate response and hijacking lipid metabolism, which likely contributes to a high chronicity rate and the pathological hallmark of steatosis in HCV infection. Cells were treated with either non-targeting control siRNA or siRNA against IKKalpha. After 72 h, cells were either mock infected or infected with HCV JFH-1 strain with the M.O.I. of 0.5.

2013-05-08 | E-GEOD-46528 | biostudies-arrayexpress

Hexokinase 3 enhances myeloid cell survival via non-glycolytic functions

Project description:Hexokinase 3 enhances myeloid cell survival via non-glycolytic functions

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Hepatitis C Virus Infection Activates a Novel Innate Pathway Involving IKKα in Lipogenesis and Viral Assembly

2013-05-08 | GSE46528 | GEO

CRISPR/Cas9 screens reveal that hexokinase 2 enhances cancer stemness and tumorigenicity

Project description:CRISPR/Cas9 screens reveal that hexokinase 2 enhances cancer stemness and tumorigenicity

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Hexokinase 2 and lactate

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Drosophila Estrogen-Related Receptor directs a transcriptional switch that supports adult glycolysis and lipogenesis

Project description:Drosophila Estrogen-Related Receptor directs a transcriptional switch that supports adult glycolysis and lipogenesis

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Drosophila Estrogen-Related Receptor directs a transcriptional switch that supports adult glycolysis and lipogenesis [ChIP-Seq]

Project description:Metabolism and development must be closely coupled to meet the changing physiological needs of each stage in the life cycle. The molecular mechanisms that link these pathways, however, remain poorly understood. Here we show that the Drosophila Estrogen-Related Receptor (dERR) directs a transcriptional switch in mid-pupae that promotes glucose oxidation and lipogenesis in young adults. dERR mutant adults are viable but display reduced locomotor activity, susceptibility to starvation, elevated glucose and an almost complete lack of stored triglycerides. Molecular profiling by RNA-seq, ChIP-seq, and metabolomics revealed that glycolytic and pentose phosphate pathway genes are induced by dERR, and their reduced expression in mutants is accompanied by elevated glycolytic intermediates, reduced TCA cycle intermediates, and reduced levels of long chain fatty acids. Unexpectedly, we find that the central pathways of energy metabolism, including glycolysis, the tricarboxylic acid cycle, and electron transport chain, are coordinately induced at the transcriptional level in mid-pupae and maintained into adulthood, and this response is partially dependent on dERR, leading to the metabolic defects observed in mutants. Our data support the model that dERR contributes to a transcriptional switch during pupal development that establishes the metabolic state of the adult fly.

2020-03-01 | GSE144763 | GEO

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