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Hexokinase 3 enhances myeloid cell survival via non-glycolytic functions

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

PROVIDER: PRJNA809305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18099966_1.fastq.gz	Fastqsanger.gz
	SRR18099966_2.fastq.gz	Fastqsanger.gz
	SRR18099967_1.fastq.gz	Fastqsanger.gz
	SRR18099967_2.fastq.gz	Fastqsanger.gz
	SRR18099968_1.fastq.gz	Fastqsanger.gz

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Hexokinase 3 enhances myeloid cell survival via non-glycolytic functions

Project description:Purpose: The goal was to compare transcriptome profiles of HL60 HK3-null and Cas9 expressing control cells treated with either ATRA or DMSO using RNA sequencing. In addition, to find accessible DNA regions by probing open chromatin with hyperactive mutant Tn5 Transposase using ATAC sequencing. Methods: HL60 HK3-null and Cas9 expressing control cells were treated with 1µM of ATRA or DMSO (0.01%) for 36h. Treated cells were then harvested for RNA-Seq and ATAC-Seq analysis. Results: We mapped sequence reads per sample to the human genome (GRCh38 - hg38) and identified differentially expressed transcripts as well as open chromatin peaks in AML HL60 HK3-null and Cas9 expressing cells upon treatment with ATRA or DMSO as control. Differentially expressed genes, were identified with a fold change ≥1.5 and FDR p-value <0.05. Conclusions: Our results show that HK3 knockout (HK3-null) AML cells had an accumulation of reactive oxygen species (ROS) as well as DNA damage during ATRA-induced differentiation. RNA sequencing analysis confirmed pathway enrichment for programmed cell death, oxidative stress and DNA damage response in HK3-null AML cells. These signatures were confirmed in ATAC sequencing, showing that loss of HK3 leads to changes in chromatin configuration and increases accessibility of genes involved in apoptosis and stress response.

2024-08-31 | GSE197164 | GEO

Fat graft survival requires metabolic reprogramming towards glycolytic pathway

Project description:Fat graft survival requires metabolic reprogramming towards glycolytic pathway

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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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Arf6 regulation of glycolytic metabolism and effector functions in neutrophils

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Fat graft survival requires metabolic reprogramming towards glycolytic pathway

Project description:Background: The mechanisms underlying fat graft survival are poorly understood. Here, we performed unbiased transcriptomics analysis of mouse fat graft model to find out the molecular mechanism of free fat graft survival. Methods: We conducted RNA-sequencing (RNA-seq) analysis of mouse free subcutaneous fat graft model at day 3 and 7 following grafting (n=5). High-throughput sequencing was performed as paired-end using NovaSeq6000 (Illumina, CA, USA). The calculated transcripts per million (TPM) values were processed for principal component analysis (PCA), unsupervised hierarchically clustered heat map generation, and Gene set enrichment analysis. Results: PCA and heat map data revealed global differences in the transcriptome of grafted fat when compared with non-graft control. The top meaningful up-regulated gene sets in the grafted fat were related to epithelial mesenchymal transition and hypoxia by day 3, and angiogenesis by day 7. Mechanistically, the glycolysis pathway was commonly upregulated in the grafted fat at day 3 (FDR q=0.012) and day 7 (FDR q=0.084). In subsequent experiments, pharmacological inhibition of glycolytic pathway in the grafted fat with 2-Deoxy-D-glucose (2-DG) significantly suppressed fat graft retention rates, both grossly and microscopically (n=5). Conclusions: Global transcriptome analysis and pharmacologic inhibition study revealed that free adipose tissue grafts undergo metabolic reprogramming towards glycolytic pathway. Whether targeting the pathway wound enhance graft survival rate remains to be investigated.

2024-06-01 | GSE203599 | GEO

Hexokinase 2 and lactate

Project description:Hexokinase 2 and lactate

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Hexokinase 2 and lactate mediated gene expression via histone H3 lysine 18 lactylation (CHO RNA-Seq)

Project description:Hexokinase catalyzes the first committed step in glucose metabolism by phosphorylating glucose to produce glucose-6-phosphate. Highly glycolytic proliferating cells such as cancer cells take advantage of HK2 expression to accelerate glucose metabolism even in the presence of oxygen. This acceleration not only provides sufficient glycolytic intermediates to support the anabolic demands of the cells but also inevitably accompanies increased formation of metabolic end products such as lactate. Currently, the effect of lactate caused by HK2-mediated metabolic alteration is largely unknown. A recent study found that lactate plays a role in an epigenetic alteration known as histone lactylation. Here, using RNA-seq and CUT&Tag chromatin profiling, we study the effect of HK2 and lactate on gene expression via histone lactylation (H3K18la).

2023-05-05 | GSE229153 | GEO

Hexokinase 2 and lactate mediated gene expression via histone H3 lysine 18 lactylation (CHO CUT&Tag)

2023-05-05 | GSE229151 | GEO

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

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

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Chemoproteomic Mapping of Glycolytic Targetome in Cancer Cells

Project description:Hyperactivated glycolysis is a metabolic hallmark of most cancer cells. Although sporadic information has revealed that glycolytic metabolites possess non-metabolic functions as signaling molecules, it remains largely elusive how these metabolites interact with and functionally regulate their binding targets. Here we introduce a Target Responsive Accessibility Profiling (TRAP) approach that measures ligand binding-induced accessibility changes for target identification through globally labeling reactive proteinaceous lysines. With TRAP, we mapped 913 responsive target candidates and 2,487 interactions for 10 major glycolytic metabolites in a model cancer cell line. The wide targetome depicted by TRAP unveils diverse regulatory modalities of glycolytic metabolites involving direct perturbation of carbohydrate metabolism enzymes, intervention of an orphan transcriptional protein’s activity, and modulation of targetome-level acetylation. These results deepen our understanding of how glycolysis orchestrates signaling pathways in cancer cells in support of their survival and inspire future exploitation of the glycolytic targetome for cancer therapy development.

2023-04-12 | GSE225738 | GEO

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