Targeting lactate metabolism for cancer therapeutics.

By J. Doherty, J. Cleveland. Journal of Clinical Investigation, 2013

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Fibroblast heterogeneity in the cancer wound (2014, background): “Because CAFs undergo changes in their metabolic activity, normalization of the metabolic phenotype and inhibition of metabolic pathways have also been suggested as a plausible way to target tumors (Witkiewicz et al., 2012; Doherty and Cleveland, 2013).”
Targeting Metabolism for Cancer Therapy (2017, background): “Substantial work has sought to target increased glycolysis including efforts to inhibit lactate production and excretion (Doherty and Cleveland, 2013; Hamanaka and Chandel, 2012; Hay, 2016; Pelicano et al., 2006; Zhao et al., 2013).”
The Science and Translation of Lactate Shuttle Theory. (2018, methodology): “, 2008), the search is on to develop MCT1 and MCT4 inhibitors (Doherty and Cleveland, 2013; Doherty et al., 2014; Draoui and Feron, 2011; Draoui et al., 2014; Sonveaux et al., 2008).”
Epithelial to Mesenchymal Transition induces cell cycle arrest and parenchymal damage in renal fibrosis (2015, neutral): “MCT4 mediates lactic acid efflux and is associated with lactate accumulation and acid microenvironment, both pro–fibrotic stimuli 38,39 .”
Foxp3 reprograms T cell metabolism to function in low glucose high lactate environments (2017, background): “LDH is already a promising drug target to interfere with cancer metabolism (Doherty and Cleveland, 2013; Xie et al., 2014).”