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Targeting the SIN1 mediated TTK/LDHA-H3K18la-GLUT3 axis disrupts metabolic-epigenetic crosstalk and suppresses progression in hyperglycolytic breast cancer.

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Cancer letters 📖 저널 OA 17.5% 2023~2026 2026 Vol.644() p. 218328 Cancer, Hypoxia, and Metabolism

TL;DR Findings link SIN1-mediated recruitment of TTK for LDHA phosphorylation to histone lactylation and GLUT3-driven metabolic reprogramming, and suggest that pharmacological disruption of this axis with LR-90, alone or in combination with standard chemotherapy, may offer a therapeutic strategy for high-glycolytic, high-lactate breast cancer.

OpenAlex 토픽 · Cancer, Hypoxia, and Metabolism Cancer Cells and Metastasis Ferroptosis and cancer prognosis

Zhao Z, Jia W, Li Z, Shi S, Zhou J, Ning C

PubMed ↗ DOI ↗ BibTeX ↓ RIS ↓

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