AI Article Synopsis
- Aspartate is essential for cancer cell metabolism, supporting protein and nucleotide synthesis while maintaining redox balance.
- Tumor cells often struggle to take up aspartate, relying on mitochondrial breakdown of glutamine to generate it.
- Various transporters facilitate this process, and losing any of them can halt cell growth in different cancers, highlighting the need to understand these metabolic pathways to identify potential treatments.
Article Abstract
Aspartate has a central role in cancer cell metabolism. Aspartate cytosolic availability is crucial for protein and nucleotide biosynthesis as well as for redox homeostasis. Since tumor cells display poor aspartate uptake from the external environment, most of the cellular pool of aspartate derives from mitochondrial catabolism of glutamine. At least four transporters are involved in this metabolic pathway: the glutamine (SLC1A5_var), the aspartate/glutamate (AGC), the aspartate/phosphate (uncoupling protein 2, UCP2), and the glutamate (GC) carriers, the last three belonging to the mitochondrial carrier family (MCF). The loss of one of these transporters causes a paucity of cytosolic aspartate and an arrest of cell proliferation in many different cancer types. The aim of this review is to clarify why different cancers have varying dependencies on metabolite transporters to support cytosolic glutamine-derived aspartate availability. Dissecting the precise metabolic routes that glutamine undergoes in specific tumor types is of upmost importance as it promises to unveil the best metabolic target for therapeutic intervention.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750728 | PMC |
| http://dx.doi.org/10.3390/cancers14010245 | DOI Listing |
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