ArticleNature communications2023
Metabolic dependencies of metastasis-initiating cells in female breast cancer.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Reinvigorating COTL1Nature cell biology · 2026Article
- Deciphering the Role of Cancer Stem Cells in Breast Cancer Brain Colonization Using a Novel Patient-Derived Model.Advanced healthcare materials · 2026Article
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- The pyruvate branch point controls lymphoid cancer cell dissemination.bioRxiv : the preprint server for biology · 2026Article
- 3D "Emboli" Culture Models Epithelial Breast Cancer Cell Oxidative Mitochondrial Metabolism with Relevance for Lung Metastasis.Cancer research communications · 2026Article
- Neutrophil Extracellular Trap Reprograms Cancer Metabolism to Form a Metastatic Niche Promoting Non-Small Cell Lung Cancer Brain Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial transfer: a new perspective on tumor-microenvironment crosstalk driving metastasis.Frontiers in immunology · 2026Review
- Exploring Lipid Metabolic Reprogramming: Mechanistic Insights and Implications for Tumor Radiotherapy.International journal of biological sciences · 2026Review
- Decoding the mechanisms underlying breast cancer brain metastasis: paving the way for precision therapeutics.Biomarker research · 2025Review
- ECM-Induced IL-23 Drives Immune Suppression in Breast Cancer via Regulating PD-1 on Tregs.Journal of experimental & clinical cancer research : CR · 2025Article
- LaGrACE: estimating gene program dysregulation with latent regulatory network.Molecular systems biology · 2025Article
- FAO-fueled OXPHOS and NRF2-mediated stress resilience in MICs drive lymph node metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Identification of potential biomarkers for breast cancer based on salivary metabolomics.Frontiers in oncology · 2025Article
- Charting the transcriptomic landscape of primary and metastatic cancers in relation to their origin and target normal tissues.Science advances · 2024Article
- Tumor Biomechanics Alters Metastatic Dissemination of Triple Negative Breast Cancer via Rewiring Fatty Acid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Hypoxic adaptation of mitochondria and its impact on tumor cell function.Seminars in cancer biology · 2024Review
- The metabolism-related lncRNA signature predicts the prognosis of breast cancer patients.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the mechanisms that enable cancer cells to metastasize is essential in preventing cancer progression. Here we examine the metabolic adaptations of metastasis-initiating cells (MICs) in female breast cancer and how those shape their metastatic phenotype. We find that endogenous MICs depend on the oxidative tricarboxylic acid cycle and fatty acid usage. Sorting tumor cells based upon solely mitochondrial membrane potential or lipid storage is sufficient at identifying MICs. We further identify that mitochondrially-generated citrate is exported to the cytoplasm to yield acetyl-CoA, and this is crucial to maintaining heightened levels of H3K27ac in MICs. Blocking acetyl-CoA generating pathways or H3K27ac-specific epigenetic writers and readers reduces expression of epithelial-to-mesenchymal related genes, MIC frequency, and metastatic potential. Exogenous supplementation of a short chain carboxylic acid, acetate, increases MIC frequency and metastasis. In patient cohorts, we observe that higher expression of oxidative phosphorylation related genes is associated with reduced distant relapse-free survival. These data demonstrate that MICs specifically and precisely alter their metabolism to efficiently colonize distant organs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.