ArticleiScience2023
Targeting metabolic fluxes reverts metastatic transitions in ovarian cancer.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Protein Variability Patterns in Ovarian Serous Carcinoma.International journal of molecular sciences · 2026Article
- Transcriptome-driven constraint-based modelling reveals metabolic targets for ovarian cancer.Cancer & metabolism · 2026Article
- Flux sampling and context-specific genome-scale metabolic models for biotechnological applications.Trends in biotechnology · 2026Review
- Distinct Chemical Cues Reprogram Cellular and Multicellular Phenotypes in Ovarian Cancer Spheroids.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- MACAW: a method for semi-automatic detection of errors in genome-scale metabolic models.Genome biology · 2025Article
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Constraint-based modelling predicts metabolic signatures of low and high-grade serous ovarian cancer.NPJ systems biology and applications · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The formation of spheroids during epithelial ovarian cancer progression is correlated with peritoneal metastasis, disease recurrence, and poor prognosis. Although metastasis has been demonstrated to be driven by metabolic changes in transformed cells, mechanistic associations between metabolism and phenotypic transitions remain ill-explored. We performed quantitative proteomics to identify protein signatures associated with three distinct phenotypic morphologies (2D monolayers and two geometrically distinct three-dimensional spheroidal states) of the high-grade serous ovarian cancer line OVCAR-3. We obtained disease-driving phenotype-specific metabolic reaction modules and elucidated gene knockout strategies to reduce metabolic alterations that could drive phenotypic transitions. Exploring the DrugBank database, we identified and evaluated drugs that could impair such transitions and, hence, cancer progression. Finally, we experimentally validated our predictions by confirming the ability of one of our predicted drugs, the neuraminidase inhibitor oseltamivir, to inhibit spheroidogenesis in three ovarian cancer cell lines without any cytotoxic effects on untransformed stromal mesothelia.
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Registered trials
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