ArticleMetabolomics : Official journal of the Metabolomic Society2025
Paclitaxel resistance-associated metabolic events in ovarian cancer cells.
Article in Metabolomics : Official journal of the Metabolomic Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Flavonoids and chalcones as selective α-glucosidase inhibitors: from enzymatic screening to validation using the human enzyme.RSC medicinal chemistry · 2026Article
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5 authors.
Funding
Abstract
introductionThe standard first-line management of advanced ovarian cancer (OC) comprises cytoreductive (debulking) surgery followed by platinum-based chemotherapy, most commonly a combination of carboplatin and paclitaxel (PTX). However, the development of resistance to PTX frequently compromises treatment efficacy, resulting in disease recurrence and poorer clinical outcomes. Although the metabolic mechanisms underlying carboplatin resistance have been extensively characterised, the specific metabolic alterations contributing to PTX resistance remain poorly understood.
objectivesWe applied untargeted metabolomics to systematically characterise PTX resistance-associated metabolic reprogramming in OC, aiming to identify targetable vulnerabilities to enhance the platinum-taxane efficacy.
methodsUsing an isogenic in vitro model of acquired PTX-resistance (OVCAR8 PTX) and its parental counterpart (OVCAR8 PAR), we analysed intracellular (endometabolome) and extracellular (exometabolome) metabolites via gas chromatography-mass spectrometry (GC-MS).
resultsMultivariate and univariate analyses (│effect size│ ≥ 1.4, p-value ≤ 0.01) revealed a distinct metabolic signature in the endometabolome of PTX-resistant cells. These cells exhibited significantly elevated levels of glycine, myo-inositol, pyroglutamate, proline and taurine, alongside reduced levels of glycerol, glucose and glutamate. Pathway analysis identified putative alterations in redox regulation (glutathione metabolism), energy metabolism (galactose and glyoxylate/dicarboxylate metabolism), amino acid metabolism (arginine and proline), and osmotic stress pathways (taurine and hypotaurine metabolism).
conclusionsThe identified metabolic signature highlights dysregulated pathways (e.g., glutathione metabolism, taurine and hypotaurine metabolism) that may be actionable targets for reversing PTX resistance. Pharmacological modulation of these pathways could restore chemosensitivity, providing a rational strategy to improve platinum-taxane efficacy in advanced OC.
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