ReviewFrontiers in cell and developmental biology2025
Metabolic reprogramming in bone metastasis of human cancers.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- The metabolic plasticity of cancer stem cells: bidirectional crosstalk with organ-resident cells.Experimental & molecular medicine · 2026Review
- Modeling and targeting the hostile physicochemical niche in bone metastasis: from experimental platforms to niche-directed therapy.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone metastasis represents a complex complication of advanced human malignancies. Metabolic reprogramming plays a critical role in bone metastasis. Tumor cells hijack and alter local metabolic pathways to fuel their energetic and biosynthetic demands for proliferation and survival within the bone metastatic microenvironment. This includes adaptations in glycolysis, oxidative phosphorylation, lipid metabolism and amino acid metabolism. Furthermore, this bone metastatic microenvironment exhibits distinct metabolic features, such as hypoxia and acidity. To survive in this hostile microenvironment, tumor cells that metastasize to bone have to undergo metabolic reprogramming. Collectively, understanding the intricate link between metabolic reprogramming and bone metastasis is crucial for developing novel therapeutic strategies. Targeting the specific metabolic addiction and interrupting the nutrient-based crosstalk between tumor cells and the bone stroma offers a promising way to inhibit the vicious cycle and bone metastatic progression.
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Registered trials
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