IlEucCana
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB55956 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR10224903.fastq.gz | Fastqsanger.gz | |||
| ERR10297774_1.fastq.gz | Fastqsanger.gz | |||
| ERR10297774_2.fastq.gz | Fastqsanger.gz | |||
| ERR10297775_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
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Project description:T-cell acute lymphoblastic leukaemia (T-ALL) is a haematological malignancy commonly driven by NOTCH1 activating mutations. A concomitant feature associated with NOTCH1 mutations is heightened oxidative metabolism enabling the exponential proliferation of T-ALL blasts. As such, targeting mitochondrial metabolism in T-ALL is an attractive therapeutic avenue. Canagliflozin (cana) is an FDA-approved sodium glucose co-transporter 2 inhibitor with known off-target effects on complex I and glutamate dehydrogenase. To date, the effects of cana on T-ALL are not known. Here, we show that cana possesses potent anti-leukaemic effects underpinned by proliferative defects, cell cycle disruption and apoptosis. These anti-leukaemic effects, driven by cana, are attributed to a perturbed tricarboxylic acid (TCA) cycle and mitochondrial metabolism and elevated mitochondrial ROS. Proteomic analysis revealed that cana treatment resulted in a compensatory increase in the expression of ATF4 targets, including upregulation of serine biosynthesis pathway and one-carbon metabolism enzymes. As such, restriction of serine and glycine synergized with cana treatment, further enhancing anti-leukaemic effects. Collectively, our study reveals cana creates a metabolic vulnerability that can be further exploited via dietary manipulation to treat T-ALL
2025-10-27 | PXD069587 | Pride
Project description:The miRNAs expression profile of four typical stages of tooth development, embryonic day 35 (E35), E45, E50, and E60, which cover the major morphological and physiological changes in pig tooth germ growth and development throughout pregnancy, including the bud, cap, early bell, and late bell stages.
2012-08-03 | GSE39848 | GEO
Project description:Sodium glucose transporter-2 inhibitors (SGLT2i) were designed to increase the excretion of glucose through urine and lower blood glucose levels independent of insulin. Beyond their primary functions, SGLT2i have been observed to induce a wide range of metabolic effects. To understand how SGLT2i-mediated metabolic changes affect skeletal metabolism, six months old genetically diverse UM-HET3 mice were treated with canagliflozin (CANA), a SGLT2i, for 1, 3, and 6 months. The comprehensive analysis included assessments of serum hormones, morphological and mechanical properties of long bones and vertebrae, and the bone tissue metabolome. The findings demonstrated significant sex-specific metabolic adaptations to CANA treatment, evident as early as one-month post-treatment. Male mice treated with CANA exhibited notable reductions in body weight, serum leptin, and insulin levels, alongside decreases in proinflammatory markers TNFα and MCP-1. These changes were accompanied by decreased serum levels of bone remodeling markers P1NP and CTX, and by reduced periosteal bone remodeling as determined by histomorphometry. The bone tissue metabolome analysis further underscored distinct sex-specific metabolic responses and adaptations to CANA treatment. Specifically, CANA-treated female mice demonstrated enhanced adenine and adenosine salvage pathways and purine metabolism relative to female controls. In contrast, CANA-treated male mice exhibited increased activity in the FXR/RXR pathway and the GABAergic receptor signaling pathways compared to their control counterparts. Notably, the most significant difference in the metabolome between CANA-treated males and females was observed in the Branched-Chain Amino Acid (BCAA) Catabolism pathway. This study highlights the novel finding of sex-specific metabolic and skeletal adaptations to SGLT2i treatment, providing new insights into the complex interplay between glucose metabolism and bone health, while emphasizing the need for tailored therapeutic strategies that consider sex-specific responses to SGLT2i treatment.
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Project description:Ovarian aging is characterized by declines in follicular reserve and the emergence of mitochondrial dysfunction, reactive oxygen species production, inflammation, and fibrosis, which eventually results in menopause. Menopause is associated with increased systemic aging and the development of numerous comorbidities; therefore, the attenuation of ovarian aging could also delay systemic aging processes in women. Recent work has established that the anti-diabetic drug Canagliflozin (Cana), a sodium-glucose transporter 2 inhibitor, elicits benefits on aging-related outcomes, likely through the modulation of nutrient-sensing pathways and metabolic homeostasis. Given that nutrient-sensing pathways play a critical role in controlling primordial follicle activation, we sought to determine if chronic Cana administration would delay ovarian aging and curtail the emergence of pathological hallmarks associated with reproductive senescence. We found that mice receiving Cana maintained their ovarian reserve through 12 months of age, which was associated with declines in primordial follicles FoxO3a phosphorylation, a marker of activation, when compared to the age-matched controls. Furthermore, Cana treatment led to decreased collagen, lipofuscin, and T cell accumulation at 12 months of age. Whole ovary transcriptomic and proteomic analyses revealed subtle improvements, predominantly in mitochondrial function and the regulation of cellular proliferation. Pathway analyses of the transcriptomic data revealed a downregulation in cell proliferation and mitochondrial dysfunction signatures, with an upregulation of oxidative phosphorylation. Pathway analyses of the proteomic data revealed declines in signatures associated with PI3K/AKT activity and lymphocyte accumulation. Collectively, we demonstrate that Cana treatment can delay ovarian aging in mice and could potentially have efficacy for delaying ovarian aging in women.
2024-12-11 | GSE283764 | GEO
Project description:We assessed the change in hepatic transciptional pattern after treatment with SGLT-2 inhibitors canagliflozin in a mice model of diet-induced obesity. Pharmacologic inhibition of the renal sodium/glucose cotransporter-2 induces glycosuria and reduces glycemia. Given that SGLT2 inhibitors (SGLT2i) reduce mortality and CV risk in T2D, improved understanding of molecular mechanisms mediating these metabolic effects is required. Treatment of obese but nondiabetic mice with the SGLT2i canagliflozin (CANA) reduces adiposity, improves glucose tolerance despite reduced plasma insulin, increases plasma ketones, and improves plasma lipid profiles. We utilized an integrated transcriptomic-metabolomics approach to demonstrate that CANA modulates key nutrient-sensing pathways, with activation of AMPK and inhibition of mTOR, independent of insulin or glucagon sensitivity or signaling. Moreover, CANA induces transcriptional reprogramming to activate catabolic pathways, increase fatty acid oxidation, reduce hepatic steatosis and diacylglycerol content, and increase hepatic and plasma levels of FGF21. Taken together, these data demonstrate that SGLT-2 inhibition triggers a fasting-like transcriptional and metabolic paradigm.
2020-04-16 | GSE148702 | GEO