ArticleMolecular systems biology2022
Sorting-free metabolic profiling uncovers the vulnerability of fatty acid β-oxidation in in vitro quiescence models.
Article in Molecular systems biology, 2022. 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, 12 citations in OpenAlex.
- A human metabolic map of pharmacological perturbations reveals drug modes of action.Nature biotechnology · 2025Article
- Cone photoreceptor phosphodiesterase PDE6H inhibition regulates cancer cell growth and metabolism, replicating the dark retina response.Cancer & metabolism · 2024Article
- Leveraging metabolic modeling and machine learning to uncover modulators of quiescence depth.PNAS nexus · 2024Article
- Identification of ATF3 as a novel protective signature of quiescent colorectal tumor cells.Cell death & disease · 2023Article
- The role of metabolism in cellular quiescence.Journal of cell science · 2023Review
- Quiescent Cancer Cells-A Potential Therapeutic Target to Overcome Tumor Resistance and Relapse.International journal of molecular sciences · 2023Review
- Sorting-free metabolic profiling uncovers the vulnerability of fatty acid β-oxidation in in vitro quiescence models.Molecular systems biology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Quiescent cancer cells are rare nondiving cells with the unique ability to evade chemotherapies and resume cell division after treatment. Despite the associated risk of cancer recurrence, how cells can reversibly switch between rapid proliferation and quiescence remains a long-standing open question. By developing a unique methodology for the cell sorting-free separation of metabolic profiles in cell subpopulations in vitro, we unraveled metabolic characteristics of quiescent cells that are largely invariant to basal differences in cell types and quiescence-inducing stimuli. Consistent with our metabolome-based analysis, we show that impairing mitochondrial fatty acid β-oxidation (FAO) can induce apoptosis in quiescence-induced cells and hamper their return to proliferation. Our findings suggest that in addition to mediating energy and redox balance, FAO can play a role in preventing the buildup of toxic intermediates during transitioning to quiescence. Uncovering metabolic strategies to enter, maintain, and exit quiescence can reveal fundamental principles in cell plasticity and new potential therapeutic targets beyond cancer.
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