Taurine from tumour niche drives glycolysis to promote leukaemogenesis

Sharma et al. 2025 — tumour-niche taurine and myeloid leukaemia

TL;DR

Bone-marrow osteolineage cells supplied taurine to taurine-transporter-dependent myeloid leukaemia cells, supporting RAG-GTP-dependent mTOR signaling and glycolysis. Genetic blockade of niche taurine production or leukaemia-cell uptake impaired disease. In mice already transplanted with blast-crisis CML, high oral taurine exposure accelerated progression. The paper supports caution in established myeloid malignancy; it does not show that ordinary supplementation initiates cancer in healthy animals or humans.

Key results

• Osteolineage CDO1-dependent taurine production increased during myeloid disease progression.
• TAUT/SLC6A6 loss impaired blast-crisis CML and AML progression, including patient-derived AML models.
• Loss of taurine uptake inhibited RAG-GTP-dependent mTOR activation and downstream glycolysis.
• In leukaemia-bearing mice on taurine-free chow, 10 mg/mL taurine in drinking water accelerated blast-crisis CML and produced an approximately threefold higher likelihood of death versus no taurine; 0.01 mg/mL was also tested (n≈14–15/group).

Evidence boundary

This is strong preclinical evidence that high exogenous taurine can accelerate established transplanted myeloid leukaemia. It is very-low-quality evidence for cancer initiation or harm from 1.5–3 g/day in a healthy human. A leukaemia-cell mTOR dependency also cannot be generalized into systemic pro-aging mTOR activation across normal tissues. gap/needs-human-replication

Limitations

• No healthy-animal cancer-incidence experiment.
• No human oral-supplementation progression or survival study in AML or blast-crisis CML.
• The 10 mg/mL drinking-water exposure is substantially above ordinary human supplement exposure after body-size scaling.

Cited by wiki pages

• taurine