Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 235, Issue 11, Pages 8757-8767Publisher
WILEY
DOI: 10.1002/jcp.29719
Keywords
breast cancer; Hv1; pHi; Warburg effect
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Funding
- Universidad Nacional de La Plata [11X/690]
- Agencia Nacional de Promocion Cientifica y Tecnologica [PICT2014-2223, PICT2016-1574]
- Consejo Nacional de Investigaciones Cientificas y Tecnicas [PIP-00340]
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Metabolic reprogramming of cancer cells results in a high production of acidic substances that must be extruded to maintain tumor-cell viability. The voltage-gated proton channel (Hv1) mediates highly selective effluxes of hydronium-ion (H+) that prevent deleterious cytoplasmic acidification. In the work described here, we demonstrated for the first time that the amino-terminal-truncated isoform of Hv1 is more highly expressed in tumorigenic breast-cancer-cell lines than in nontumorigenic breast cells. With respect to Hv1 function, we observed that pharmacologic inhibition of that channel, mediated by the specific blocker 5-chloro-2-guanidinobenzimidazole, produced a drop in intracellular pH and a decrease in cell viability, both in monolayer and in three-dimensional cultures, and adversely affected the cell-cycle in tumorigenic breast cells without altering the cycling of nontumorigenic cells. In conclusion, our results demonstrated that the Hv1 channel could be a potential tool both as a biomarker and as a therapeutic target in breast-cancer disease.
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