Cobalamin Metabolism Is a Key Process of Breast Cancer Cells That Offers New Ways for Diagnosis and Treatment
Cobalamin, also known as vitamin B12, is an essential cofactor involved in one-carbon metabolism, mitochondrial function, and epigenetic regulation. As humans rely entirely on dietary intake of cobalamin paired with a highly coordinated absorption and transportation system, disruptions to this metabolic process can have profound health consequences. Breast cancer, the most frequently diagnosed malignancy among women worldwide, exhibits distinct metabolic adaptations, including altered cobalamin uptake and dependency on B12-driven biochemical pathways. This review summarizes the molecular mechanisms governing cobalamin metabolism, with a focus on absorption, transport, and intracellular processes relevant to breast cancer biology. We then examine how breast cancer cells reprogram these pathways. Finally, we evaluate emerging pharmaceutical strategies that target cobalamin metabolism, including B12-based imaging probes, cobalamin-conjugated drug delivery systems, and inhibitors of B12-dependent enzymes. Although these approaches show promise, further research is needed to define subtype-specific metabolic signatures, optimize cobalamin-mediated drug targeting, and clarify how systemic B12 status influences therapeutic response. By integrating biochemical, epidemiological, and translational perspectives, this review outlines how cobalamin-centered strategies may contribute to more precise diagnostic and therapeutic options for breast cancer.
Authors
- Jorge L. Gutiérrez-Pajares (ORCID: https://orcid.org/0000-0002-3573-0754)
- Isabel Gómez-Betancur
- Francisco León
Institutions
- University of South Carolina (US)
- Universidad Bernardo O'Higgins (CL)
- Federación Colombiana de Obstetricia y Ginecología (CO)
Publication Details
- Journal
- Scientia Pharmaceutica
- Published
- 2026-02-17
- DOI
- https://doi.org/10.3390/scipharm94010018
- Primary Topic
- Folate and B Vitamins Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00