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MiRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [miRNA]

ABSTRACT: miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [miRNA]

PROVIDER: PRJNA908842 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22535666.fastq.gz	Fastqsanger.gz
	SRR22535667.fastq.gz	Fastqsanger.gz
	SRR22535668.fastq.gz	Fastqsanger.gz
	SRR22535669.fastq.gz	Fastqsanger.gz
	SRR22535670.fastq.gz	Fastqsanger.gz

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miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation

Project description:miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation

| PRJNA908841 | ENA

miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [mRNA]

Project description:miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [mRNA]

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miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [miRNA]

Project description:Acute myeloid leukemia (AML) is a heterogeneous and deadly disease characterized by uncontrolled expansion of malignant blasts. The current treatment for AML patients includes intensive chemotherapy and high-risk hematopoietic stem cell transplantation, highlighting the need for less toxic and more effective therapies. Altered metabolism and dysregulated microRNA (miRNA) expression profiles are characteristic of AML. However, there is a paucity of studies exploring how changes in the metabolic state of the leukemic cells regulate miRNA expression leading to altered cellular behavior. Here, we blocked pyruvate entry into mitochondria by deleting the Mitochondria Pyruvate Carrier (MPC1) gene in MV4-11 and Molm-14 human AML cell lines, which decreased Oxidative Phosphorylation (OXPHOS). The loss of MPC1 led to increased expression of miR-1 in both human AML cell lines tested. AML patient sample analysis showed that higher miR-1 expression correlates with reduced survival. Transcriptional and metabolic profiling of miR-1 overexpressing AML cells revealed that miR-1 increased OXPHOS, along with key metabolites that fuel the TCA cycle such as glutamine and fumaric acid. Inhibition of glutaminolysis decreased the elevated OXPHOS in miR-1 overexpressing MV4-11 cells, highlighting that miR-1 regulates OXPHOS through glutaminolysis. Further, the overexpression of miR-1 in AML cells exacerbated disease in a mouse xenograft model. Our work expands current knowledge within the field by uncovering novel connections between AML cell metabolism and miRNA expression that facilitates disease progression. Together, our work points to miR-1 as a potential new therapeutic target that can be used to disrupt AML cell metabolism and thus pathogenesis.

2023-08-11 | GSE220133 | GEO

miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [mRNA]

2023-08-11 | GSE220126 | GEO

miRNA-1 promotes acute myeloid leukemia cell pathogenesis through metabolic regulation.

Project description:Acute myeloid leukemia (AML) is a heterogeneous and deadly disease characterized by uncontrolled expansion of malignant blasts. Altered metabolism and dysregulated microRNA (miRNA) expression profiles are both characteristic of AML. However, there is a paucity of studies exploring how changes in the metabolic state of the leukemic cells regulate miRNA expression leading to altered cellular behavior. Here, we blocked pyruvate entry into mitochondria by deleting the Mitochondria Pyruvate Carrier (MPC1) gene in human AML cell lines, which decreased Oxidative Phosphorylation (OXPHOS). This metabolic shift also led to increased expression of miR-1 in the human AML cell lines tested. AML patient sample datasets showed that higher miR-1 expression correlates with reduced survival. Transcriptional and metabolic profiling of miR-1 overexpressing AML cells revealed that miR-1 increased OXPHOS, along with key metabolites that fuel the TCA cycle such as glutamine and fumaric acid. Inhibition of glutaminolysis decreased OXPHOS in miR-1 overexpressing MV4-11 cells, highlighting that miR-1 promotes OXPHOS through glutaminolysis. Finally, overexpression of miR-1 in AML cells exacerbated disease in a mouse xenograft model. Together, our work expands current knowledge within the field by uncovering novel connections between AML cell metabolism and miRNA expression that facilitates disease progression. Further, our work points to miR-1 as a potential new therapeutic target that may be used to disrupt AML cell metabolism and thus pathogenesis in the clinic.

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HDAC2-mediated miRNA profiling in acute myeloid leukemia

Project description:miRNA microarray expression analysis of human acute myeloid leukemia cell line (U937) after HDAC2 genetically and enzymatically defection

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HDAC2-mediated miRNA profiling in acute myeloid leukemia

Project description:HDAC2-mediated miRNA profiling in acute myeloid leukemia

| PRJNA530245 | ENA

Proteogenomic pathogenesis and classification of acute myeloid leukemia

Project description:Acute myeloid leukemia is a clinically and genetically heterogenous disease characterized by bone marrow infiltration with immature leukemic blasts that cause bone marrow failure. Patient age, comorbidities and genomic disease characteristics have a profound impact on patient outcome. Here, we present an integrated Multi-Omics analysis of protein and gene expression as well as cytogenetics and mutations to capture the rewiring of intracellular protein networks that is most likely caused by genomic aberrations. Because protein networks are downstream of genomic aberrations, we hypothesized that our Multi-Omics approach may add to the current AML classification by identifying proteomic AML subtypes with specific clinical and molecular features that could identify therapeutic vulnerabilities and aid in the identification of predictive biomarkers.

2022-03-08 | PXD023090 | Pride

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miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-11 | GSE220134 | GEO