A novel Na_v1.5-dependent feedback mechanism driving glycolytic acidification in breast cancer metastasis.

ABSTRACT: Solid tumours have abnormally high intracellular [Na⁺]. The activity of various Na⁺ channels may underlie this Na⁺ accumulation. Voltage-gated Na⁺ channels (VGSCs) have been shown to be functionally active in cancer cell lines, where they promote invasion. However, the mechanisms involved, and clinical relevance, are incompletely understood. Here, we show that protein expression of the Na_v1.5 VGSC subtype strongly correlates with increased metastasis and shortened cancer-specific survival in breast cancer patients. In addition, VGSCs are functionally active in patient-derived breast tumour cells, cell lines, and cancer-associated fibroblasts. Knockdown of Na_v1.5 in a mouse model of breast cancer suppresses expression of inva

SUBMITTER: Leslie TK 

PROVIDER: S-EPMC11329375 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature