Slc16a3, also named as MCT4, is a transporter encoding monocarboxylate transporter 4, which mediates lactic acid efflux across the plasma membrane [1,4,6]. It is involved in energy metabolism pathways, especially glycolysis, and is crucial for maintaining the metabolic balance of tumor cells [1,6]. Genetic models such as gene knockout (KO) mouse models can be valuable for studying its functions in vivo.

Knockdown of Slc16a3 in tumor cells, including hepatocellular carcinoma and B16-F10 cells, reduces glycolytic activity and lactic acid production [1,3]. In bladder cancer, high Slc16a3 expression is related to poor prognosis, and it may influence immune infiltration by regulating metabolism and m6A methylation [2]. In lung cancer, SLC16A3 is significantly upregulated, associated with immunosuppressive cells and factors, and may contribute to a worse prognosis through the HIF-1α-IL8 axis [5].

In conclusion, Slc16a3 is vital in energy metabolism, especially in glycolysis-related lactic acid transport. Studies using KO or knockdown models in various cancer types, such as hepatocellular, bladder, and lung cancers, have revealed its role in tumor-related processes like metabolism, immune regulation, and prognosis. Understanding Slc16a3 functions provides potential therapeutic targets for cancer treatment [1,2,3,5].