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Induction of a timed metabolic collapse to overcome cancer chemoresistance

ABSTRACT: Induction of a timed metabolic collapse to overcome cancer chemoresistance

PROVIDER: PRJNA578674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10317115.fastq.gz	Fastqsanger.gz
	SRR10317116.fastq.gz	Fastqsanger.gz
	SRR10317117.fastq.gz	Fastqsanger.gz
	SRR10317118.fastq.gz	Fastqsanger.gz
	SRR10317119.fastq.gz	Fastqsanger.gz

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Induction of a timed metabolic collapse to overcome cancer chemoresistance

Project description:We identified a transient increase in metabolites involved in glutamine metabolism in chemoresistant acute myeloid leukemia (AML) cells. To further investigate this, we evaluated the transcriptome of AML cells from bone marrow of vehicle-treated mice and mice treated with induction chemotherapy (doxorubicin+cytarabine) at 3 days (iCT group) and 10 days (relapse group) after completion of the chemotherapy.

2020-08-05 | GSE139159 | GEO

Induction of a Timed Metabolic Collapse to Overcome Cancer Chemoresistance.

Project description:Cancer relapse begins when malignant cells pass through the extreme metabolic bottleneck of stress from chemotherapy and the byproducts of the massive cell death in the surrounding region. In acute myeloid leukemia, complete remissions are common, but few are cured. We tracked leukemia cells in vivo, defined the moment of maximal response following chemotherapy, captured persisting cells, and conducted unbiased metabolomics, revealing a metabolite profile distinct from the pre-chemo growth or post-chemo relapse phase. Persisting cells used glutamine in a distinctive manner, preferentially fueling pyrimidine and glutathione generation, but not the mitochondrial tricarboxylic acid cycle. Notably, malignant cell pyrimidine synthesis also required aspartate provided by specific bone marrow stromal cells. Blunting glutamine metabolism or pyrimidine synthesis selected against residual leukemia-initiating cells and improved survival in leukemia mouse models and patient-derived xenografts. We propose that timed cell-intrinsic or niche-focused metabolic disruption can exploit a transient vulnerability and induce metabolic collapse in cancer cells to overcome chemoresistance.

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Targeting cell cycle and apoptosis to overcome chemoresistance in AML

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Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

Project description:Chemoresistance poses a significant challenge in treating non-small cell lung cancer (NSCLC), often leading to poor outcomes. This resistance is closely linked to cancer stem cell (CSC)-like characteristics, including the ability to evade anoikis. In this study, we identified dual-specificity phosphatase 23 (DUSP23) as a key molecule involved in regulating CSC traits and chemoresistance. DUSP23 expression was significantly elevated in cell clusters grown under ultra-low adhesion (ULA) conditions that mimic CSC-promoting environments. Silencing DUSP23 reduced the formation of these clusters, suppressed the expression of the stemness markers SOX2, and enhanced anoikis sensitivity. Additionally, in cisplatin-resistant NSCLC cells, knockdown of DUSP23 decreased invasive behavior and induced apoptosis. These findings suggest that DUSP23 plays a pivotal role in maintaining CSC-like properties and chemoresistance by regulating SOX2. Targeting DUSP23 could offer a novel approach to overcome treatment resistance and improve outcomes for patients with NSCLC.

2025-01-31 | GSE288032 | GEO

Induction of fatty acid oxidation underlies DNA damage-induced cell death and ameliorates obesity-driven chemoresistance

Project description:The DNA damage response is essential for preserving genome integrity and eliminating damaged cells. Although cellular metabolism plays a central role in cell fate decision between proliferation, survival or death, the metabolic response to DNA damage remains largely obscure. Here, we show that DNA damage induces fatty acid oxidation (FAO), which is required for DNA damage-induced cell death. Mechanistically, FAO induction increases cellular acetyl-CoA levels and promotes N-alpha-acetylation of caspase-2, leading to cell death. Whereas chemotherapy increases FAO related genes through PPARα, accelerated hypoxia-inducible factor-1α stabilization by tumor cells in obese mice impedes the upregulation of FAO, which contributes to its chemoresistance. Finally, we find that improving FAO by PPARα activation ameliorates obesity-driven chemoresistance and enhances the outcomes of chemotherapy in obese mice. These findings reveal the shift toward FAO induction is an important metabolic response to DNA damage and may provide effective therapeutic strategies for cancer patients with obesity.

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Cellular proteostasis collapse in mammalian senescence

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Uncovering early response of gene regulatory networks in ES cells by systematic induction of transcription factors

Project description:This SuperSeries is composed of the following subset Series: GSE14559: Timed induction of 50 transcription factors in ES cells reveals a common mechanism to initiate differentiations GSE14586: Cdx2 Binding Sites On Cdx2 Expressing ES Cells GSE16148: Timed induction of 10 transcription factors - ES time series data Refer to individual Series

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Project description:Metabolic reprogramming, carried out by cancer cells to rapidly adapt to stress such as hypoxia and limited nutrient conditions, is an emerging concepts in tumor biology, and is now recognized as one of the hallmarks of cancer. In contrast with conventional views, based on the classical Warburg effect, these metabolic alterations require fully functional mitochondria and finely-tuned regulations of their activity. In turn, the reciprocal regulation of the metabolic adaptations of cancer cells and the microenvironment critically influence disease progression and response to therapy. This is also realized through the function of specific stress-adaptive proteins, which are able to relieve oxidative stress, inhibit apoptosis, and facilitate the switch between metabolic pathways. Among these, the molecular chaperone tumor necrosis factor receptor associated protein 1 (TRAP1), the most abundant heat shock protein 90 (HSP90) family member in mitochondria, is particularly relevant because of its role as an oncogene or a tumor suppressor, depending on the metabolic features of the specific tumor. This review highlights the interplay between metabolic reprogramming and cancer progression, and the role of mitochondrial activity and oxidative stress in this setting, examining the possibility of targeting pathways of energy metabolism as a therapeutic strategy to overcome drug resistance, with particular emphasis on natural compounds and inhibitors of mitochondrial HSP90s.

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Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

Project description:Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

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The essential role of PBX1, a stem cell reprogramming factor, in ovarian cancer chemoresistance

Project description:Elucidating the pathogenesis of chemoresistance is fundamental for developing more effective interventions that will improve the clinical outcome of neoplastic diseases such as ovarian cancer. Here, we report the upregulation of PBX1, a stem cell reprogramming factor, in recurrent ovarian carcinomas. Moreover, high levels of PBX1 expression are correlated with a shorter survival rate among post-chemotherapy ovarian cancer patients. Ectopic expression of PBX1 promotes cancer stem cell-like phenotypes, including increased side population and ALDH activity, enhanced tumorigenicity at a low cell density, and increased resistance to platinum-based therapy. Silencing PBX1 in platinum-resistant cell lines that overexpress PBX1 sensitizes cells to platinum treatment and reduces their â??stemnessâ??. Analysis of previously reported genome-wide chromatin immunoprecipitation data shows that PBX1 binds directly to promoters of genes involved in stem cell maintenance and tissue injury response. We confirmed direct regulation of STAT3 by PBX1, and demonstrated that the PBX1 binding motif located on the STAT3 promoter participates in positive transcriptional regulation of STAT3. Furthermore, a STAT3/JAK2 inhibitor potently sensitizes platinum-resistant cells to carboplatin and suppresses their growth in vivo. These findings establish PBX1 as an upstream regulator of key pathways in stem cell and tissue damage response and highlight the potential of targeting the PBX1/STAT3 axis to overcome chemoresistance in human cancers. Determine gene expression changes after knockdown of PBX1 protein in an ovarian cancer cell line (OVCAR3)

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