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Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells

ABSTRACT: Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells

PROVIDER: PRJNA686363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13272050_1.fastq.gz	Fastqsanger.gz
	SRR13272050_2.fastq.gz	Fastqsanger.gz
	SRR13272051_1.fastq.gz	Fastqsanger.gz
	SRR13272051_2.fastq.gz	Fastqsanger.gz
	SRR13272052_1.fastq.gz	Fastqsanger.gz

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Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells

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Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells.

Project description:Acute myeloid leukaemia (AML) cells interact and modulate components of their surrounding microenvironment into their own benefit. Stromal cells have been shown to support AML survival and progression through various mechanisms. Nonetheless, whether AML cells could establish beneficial metabolic interactions with stromal cells is underexplored. By using a combination of human AML cell lines and AML patient samples together with mouse stromal cells and a MLL-AF9 mouse model, here we identify a novel metabolic crosstalk between AML and stromal cells where AML cells prompt stromal cells to secrete acetate for their own consumption to feed the tricarboxylic acid cycle (TCA) and lipid biosynthesis. By performing transcriptome analysis and tracer-based metabolic NMR analysis, we observe that stromal cells present a higher rate of glycolysis when co-cultured with AML cells. We also find that acetate in stromal cells is derived from pyruvate via chemical conversion under the influence of reactive oxygen species (ROS) following ROS transfer from AML to stromal cells via gap junctions. Overall, we present a unique metabolic communication between AML and stromal cells and propose two different molecular targets, ACSS2 and gap junctions, that could potentially be exploited for adjuvant therapy.

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Selective Dependence on Stromal Acetate induced Polyamine Metabolism Provides Unique Therapeutic Opportunities in Pancreatic Cancer

Project description:The ability of tumor cells to thrive in harsh microenvironments depends on the utilization of nutrients available in the milieu. However, the signaling and nutritional potential of the stromal cell-secreted metabolites remains poorly understood. We identified a novel metabolic crosstalk between cancer associated fibroblasts (CAFs) and pancreatic cancer cells. We demonstrate that pancreatic CAFs regulate tumor cell metabolism through the secretion of acetate, which can be blocked by silencing ACLY in CAFs. Cancer cells present a unique dependence on CAF-derived acetate under acidosis. We further show that ACSS2 channels the exogenous acetate to regulate the dynamic cancer epigenome and transcriptome, thereby facilitating cancer cell survival in the acidic microenvironment. Comparative H3K27ac ChIP-Seq and RNA-Seq analyses revealed alterations in polyamine homeostasis through regulation of SAT1 gene expression and enrichment of the SP1-responsive signature. We observed novel acetate/ACSS2-mediated acetylation of SP1 at lysine 19 residue that increased SP1 protein stability and transcriptional activity. Genetic or pharmacologic inhibition of the ACSS2-SP1-SAT1 axis diminished tumor burden in mouse models. Increased SAT1-mediated production of N1-acetylspermidine correlated with disease progression in the spontaneous tumor progression model and poor survival in cancer patients. These results reveal that the metabolic flexibility imparted by the stroma-derived acetate enabled cancer cell survival under acidosis via the ACSS2-SP1-SAT1 axis.

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