ArticleCell metabolism2019
Cell Clustering Promotes a Metabolic Switch that Supports Metastatic Colonization.
Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 142 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
142 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026Pooled it
- Kaempferide in Alpinia officinarum Hance Exerts Anti-Hepatocellular Carcinoma Activity by Inhibiting Mitophagy Through Downregulation of BNIP3L.Journal of cellular and molecular medicine · 2026Article
- Metabolic plasticity and optimal redox homeostasis are essential for efficient metastatic colonization.Molecular metabolism · 2026Article
- AnGenes · 2026Article
- Article
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- A GPX1-OSBPL8 axis mediates noncanonical in vivo ferroptosis and cancer growth suppression.Cell · 2026Article
- The pyruvate branch point controls lymphoid cancer cell dissemination.bioRxiv : the preprint server for biology · 2026Article
- Absolute dynamic and relative static: the relationship of glycolysis and OXPHOS in cancer development.Cell death discovery · 2026Review
- Extracellular matrix mediates circulating tumor cell clustering in triple-negative breast cancer metastasis.Nature communications · 2026Article
- Exploring metabolic dynamics of cancer metastasis through in vitro models.Discover oncology · 2026Review
- Tight junction-high and CDH17-positive cell population is the source of colorectal cancer liver metastases.Nature communications · 2026Article
- Interplay of oxidative stress and antioxidant mechanisms in cancer development and progression.Archives of toxicology · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- A feedback loop between cell proliferation and ROS regulates ferroptosis sensitivity.Frontiers in cell and developmental biology · 2026Article
- Compression-induced NF-κB activation sustains tumor cell survival in confinement by detoxifying aldehydes and promotes metastasis.Nature communications · 2025Article
- Unfolded protein response kinase PERK supports survival and metastasis of circulating tumor cell clusters via SAM synthesis and H3K4me3-dependent PDGFB signaling.Cancer communications (London, England) · 2025Article
- Inducing ferroptosis to impede metastasis by inhibiting the calcium channel TRPC6.Cell reports · 2025Article
- Circulating tumor cells: mechanisms and clinical significance in colorectal cancer metastasis.Molecular cancer · 2025Review
- Collective migration modes in development, tissue repair and cancer.Nature reviews. Molecular cell biology · 2025Review
82 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cancer metastasis depends on cell survival following loss of extracellular matrix attachment and dissemination through the circulation. The metastatic spread can be enhanced by the clustering of detached cancer cells and increased antioxidant defense. Here, we link these responses by describing how cell clustering limits reactive oxygen species (ROS). Loss of attachment causes mitochondrial perturbations and increased ROS production. The formation of cell clusters induces a hypoxic environment that drives hypoxia-inducible factor 1-alpha (Hif1α)-mediated mitophagy, clearing damaged mitochondria and limiting ROS. However, hypoxia and reduced mitochondrial capacity promote dependence on glycolysis for ATP production that is supported by cytosolic reductive metabolism. Preventing this metabolic adaptation or disruption of cell clusters results in ROS accumulation, cell death, and a reduction of metastatic capacity in vivo. Our results provide a mechanistic explanation for the role of cell clustering in supporting survival during extracellular matrix detachment and metastatic spread and may point to targetable vulnerabilities.
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Registered trials
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.