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The effects of lactate and its transporters on tumors and immunity and advances in the corresponding treatment
Bai Rilan, Bai Ling, Li Wei, Cui Jiuwei
Cancer Center, the First Hospital of Jilin University, Changchun 130021, Jilin, China
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Abstract  Tumor metabolic reprogramming confers competitive advantages to its survival and progression, one of the important features being increased lactate production caused by the aerobic glycolytic, "Warburg" effect. Lactate and its transport receptors, monocarboxylate transporters (MCTs), especially MCT1 and MCT4 subtypes, play an essential role in the biological activity of tumors and immune cells. On one hand, the tumor microenvironment acidified by lactate contributes to the migration and invasion of tumor cell, angiogenesis and escape to immune surveillance; and MCT1/4, as the indispensable porter of lactate, play an essential role in metabolic adaptations, metabolic symbiosis, and maintenance of the metabolic phenotype of cancer cells, as well as tumor malignant activities. on the other hand, lactate itself and the process of lactate transport mediated by MCTs also affect the activity and differentiation of immune cells. In recent years, inhibitors targeting MCTs in lactate metabolism seem to be promising means of cancer treatment, and although immune cells may be affected to varying degrees, some breakthroughs have been made in the gradual exploration as a whole. This article provides an overview of the relationship between lactate and its transporters with the tumor and immune microenvironment. It also explores the possibility of therapeutic strategies targeting MCTs in lactate metabolism.
Key wordsCancer      Lactate      Monocarboxylate transporter      Immune regulation      Inhibitor     
Received: 15 February 2021     
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Bai Rilan
Bai Ling
Li Wei
Cui Jiuwei
Cite this article:   
Bai Rilan,Bai Ling,Li Wei, et al. The effects of lactate and its transporters on tumors and immunity and advances in the corresponding treatment[J]. Electron J Metab Nutr Cancer, 2021, 8(3): 245-250.
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http://182.92.200.144/EN/     OR     http://182.92.200.144/EN/Y2021/V8/I3/245
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