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Peer-reviewedCC BY-NC-NDCell communication and signaling : CCS

Glutamine as a context-dependent regulator controlling metabolism and immunity in triple-negative breast cancer.

  • Anam Aftab1
  • Marilena Pontoriero2
  • Marina La Chimia2
  • Luca Gallelli3
  • Domenica Scumaci4
4 affiliations
  1. 1Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy. [email protected].
  2. 2Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
  3. 3Department of Health Sciences, Magna Graecia University of Catanzaro, Catanzaro, Italy.
  4. 4Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy. [email protected].
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Abstract

Background

Triple-negative breast cancer (TNBC) exhibits early metastasis, a unique metabolic rigidity and poor clinical outcomes. A substantial, biomarker-definable subset of TNBC depends on glutamine metabolism, which can act as a nutrient source and a regulator of proliferation, redox homeostasis, epigenetic remodelling, and immune evasion.Main body

Glutamine metabolism in TNBC involves several interrelated processes, including transporter regulation, transcriptional control (FOXM1/FUS/SLC7A5 axis), and organelle-specific redox adaptation (ER-PPP/H6PD pathway). Various transporters mediate the uptake of glutamine into the cells. Once inside the cells, glutamine undergoes enzymatic conversion, driving essential metabolic pathways that support the tumor's energy needs, maintain cellular redox balance, and drive epigenetic changes that promote cancer progression. Furthermore, the tumor microenvironment, including spatial immune-metabolic competition/heterogeneity, is significantly influenced by glutamine metabolism. The availability of glutamine can regulate the behavior of immune cells, including T cells and macrophages, potentially leading to immune suppression and contributing to therapeutic resistance.Conclusion

We concluded that glutamine metabolism is a key dependency in a substantial, biomarker-definable subset of TNBC. The therapeutic potential of glutamine metabolism not only offers a promising avenue for improving treatment outcomes but also presents a means to overcome current therapeutic limitations in TNBC.

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Cite

BibTeXRIS
BibTeX
@article{aftab2026glutamine,
  title = {{Glutamine as a context-dependent regulator controlling metabolism and immunity in triple-negative breast cancer.}},
  author = {Anam Aftab and Marilena Pontoriero and Marina La Chimia and Luca Gallelli and Domenica Scumaci},
  journal = {Cell communication and signaling : CCS},
  year = {2026},
  month = aug,
  doi = {10.1186/s12964-026-03150-1},
  url = {https://europepmc.org/article/MED/43010005},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Glutamine as a context-dependent regulator controlling metabolism and immunity in triple-negative breast cancer.
AU  - Anam Aftab
AU  - Marilena Pontoriero
AU  - Marina La Chimia
AU  - Luca Gallelli
AU  - Domenica Scumaci
PY  - 2026
DA  - 2026/08/13
JO  - Cell communication and signaling : CCS
DO  - 10.1186/s12964-026-03150-1
UR  - https://europepmc.org/article/MED/43010005
AB  - Background  Triple-negative breast cancer (TNBC) exhibits early metastasis, a unique metabolic rigidity and poor clinical outcomes. A substantial, biomarker-definable subset of TNBC depends on glutamine metabolism, which can act as a nutrient source and a regulator of proliferation, redox homeostasis, epigenetic remodelling, and immune evasion.Main body  Glutamine metabolism in TNBC involves several interrelated processes, including transporter regulation, transcriptional control (FOXM1/FUS/SLC7A5 axis), and organelle-specific redox adaptation (ER-PPP/H6PD pathway). Various transporters mediate the uptake of glutamine into the cells. Once inside the cells, glutamine undergoes enzymatic conversion, driving essential metabolic pathways that support the tumor's energy needs, maintain cellular redox balance, and drive epigenetic changes that promote cancer progression. Furthermore, the tumor microenvironment, including spatial immune-metabolic competition/heterogeneity, is significantly influenced by glutamine metabolism. The availability of glutamine can regulate the behavior of immune cells, including T cells and macrophages, potentially leading to immune suppression and contributing to therapeutic resistance.Conclusion  We concluded that glutamine metabolism is a key dependency in a substantial, biomarker-definable subset of TNBC. The therapeutic potential of glutamine metabolism not only offers a promising avenue for improving treatment outcomes but also presents a means to overcome current therapeutic limitations in TNBC.
SN  - 1478-811X
ER  -