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MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress

ABSTRACT: MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress

PROVIDER: PRJNA714389 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13960560.fastq.gz	Fastqsanger.gz
	SRR13960561.fastq.gz	Fastqsanger.gz
	SRR13960562.fastq.gz	Fastqsanger.gz
	SRR13960563.fastq.gz	Fastqsanger.gz
	SRR13960564.fastq.gz	Fastqsanger.gz

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Similar Datasets

MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [array]

Project description:MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [array]

| PRJNA714388 | ENA

MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [ChIP-seq]

Project description:MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [ChIP-seq]

| PRJNA714385 | ENA

MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [array]

Project description:MondoA (also known as MLXIP), a member of the MYC interactome, has been described as an example of a metabolic sensor. By assessing patient data sets we found that MondoA overexpression is associated with a worse survival in pediatric common acute lymphoblastic leukemia (B-ALL). Using CRISPR/Cas9 and RNA interference approaches, we observed that MondoA depletion reduces transformational capacity of B-ALL cells in vitro and dramatically inhibits malignant potential in an in vivo mouse model. Interestingly, reduced expression of MondoA in patient data sets correlated with enrichment in metabolic pathways. The loss of MondoA correlated with increased tricarboxylic acid (TCA) cycle activity. Mechanistically, MondoA senses metabolic stress in B-ALL cells by restricting oxidative phosphorylation through reduced PDH activity. Glutamine starvation conditions greatly enhance this effect and highlight the inability to mitigate metabolic stress upon loss of MondoA in B-ALL. CHIPseq revealed a modest but highly significant redistribution of MYC towards binding sites shared with MondoA upon loss of MondoA.

2021-04-04 | GSE168865 | GEO

MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress [ChIP-seq]

2021-04-04 | GSE168864 | GEO

MondoA drives malignancy in B-ALL through enhanced adaptation to metabolic stress.

Project description: Not available

| S-EPMC11017790 | biostudies-literature

MondoA Drives Malignancy in B-ALL through Enhanced Adaptation to Metabolic Stress

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

2021-04-04 | GSE168866 | GEO

Deregulated Myc Requires MondoA for Metabolic Reprogramming and Tumorigenesis

Project description:In order to investigate the effect of MondoA loss on the expression of Myc-dependent genes, we performed a microarray analysis from RNAs isolated from TET21N cells expressing either control (siControl) or MondoA (siMondoA) siRNAs either with (NT) or without (Doxy) induced N-Myc expression. TET21N cells were grown in medium with either Doxy (Myc-Off) or No Treatment (Myc-On), then transiently transfected with either non-specific siRNA or MondoA siRNA in replicates. Cells were then lysed and RNA isolated.

2015-01-01 | E-GEOD-55538 | biostudies-arrayexpress

Deregulated Myc Requires MondoA for Metabolic Reprogramming and Tumorigenesis

2015-01-01 | GSE55538 | GEO

MondoA is highly expressed in acute lymphoblastic leukemia and modulates metabolism, differentiation and survival

Project description:Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. To identify novel candidates for targeted treatment of childhood ALL, we performed a comprehensive transcriptome analysis yielding a set of genes specifically overexpressed in ALL. Among them we identified MondoA - a transcription factor regulating glycolysis in response to glucose availability. Here, we confirm that MondoA is highly overexpressed ALL, whereas the MondoA paralog, MondoB, is not expressed. Expression studies revealed that MondoA is not regulated by glucose availability in leukemia cells, but by the presence of lactate. An in silico MondoA promoter analysis identified two methylation-prone CpG-islands and four conserved binding sites for runt-related transcription factor 1 (RUNX1). In fact, MondoA and RUNX1 are significantly coexpressed in leukemia and experimental blockage of DNA methylation leads to a further induction of MondoA. In addition, using microarray profiling, gene-set enrichment analysis and RNA interference we provide for the first time evidence that MondoA expression not only increases glucose catabolism, but also maintains a more immature ALL phenotype, which is associated with enhanced survival and clonogenicity of leukemia cells. These data hint to an important contribution of MondoA to leukemia aggressiveness validating MondoA as an attractive candidate for targeted treatment of ALL. Two nonsense shRNA expressing control Nalm6 clones and three MondoA shRNA expressing Nalm6 clones were subjected to microarray analysis.

2012-07-31 | E-GEOD-33967 | biostudies-arrayexpress

Age-associated decline of MondoA drives cellular senescence through impaired autophagy and mitochondrial homeostasis

Project description:Accumulation of senescent cells affects organismal aging and the prevalence of age-associated disease. Emerging evidence suggests that activation of autophagy protects against age-associated diseases and promotes longevity, but the roles and regulatory mechanisms of autophagy in cellular senescence are not well understood. Here we identified the transcription factor, MondoA, as a novel regulator of cellular senescence, autophagy and mitochondrial homeostasis. MondoA protected against cellular senescence by activating autophagy partly through the suppression of an autophagy negative regulator, Rubicon. In addition, we identified peroxiredoxin 3 (Prdx3) as another downstream regulator of MondoA essential for mitochondrial homeostasis and autophagy. Rubicon and Prdx3 worked independently to regulate senescence. Furthermore, we found that MondoA knockout mice had exacerbated senescence during ischemic acute kidney injury (AKI), and a decrease of MondoA in the nucleus was correlated with human aging and ischemic AKI. Our results suggest that retaining MondoA activity protects from senescence and age-associated disease.

2022-03-01 | GSE179016 | GEO

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