Slc2a6, also known as GLUT6, is a member of the solute carrier 2 family. It is involved in multiple biological processes such as glucose transport and is associated with pathways like glycolysis, immune response, and ferroptosis [1,3,4]. Genetic models, especially KO mouse models, are valuable for studying its functions.

In myoblast differentiation, Slc2a6 is up-regulated during normal differentiation but down-regulated in diabetes-induced muscle atrophy. RNAi of Slc2a6 in C2C12 myoblasts impairs differentiation and myotube formation, with differentially expressed genes and metabolites enriched in the glycolysis pathway. It regulates myogenic differentiation partly through the glycolysis pathway by targeting LDHB [1].

In breast cancer, overexpression of SLC2A6 can inhibit tumor cell proliferation, promote mitochondrial damage, and induce apoptosis, acting as a tumor suppressor [2].

In Japanese flounder, slc2a6 is involved in viral regulation by regulating innate immune responses, with its expression increased after lymphocystis disease virus stimulation [3].

In hepatocellular carcinoma, knockdown of SLC2A6 suppresses cell proliferation, migration, and invasion, closely related to the ferroptosis pathway [4].

In conclusion, Slc2a6 plays essential roles in processes like myoblast differentiation, immune response, and cancer development. Studies using KO/CKO mouse models and other loss-of-function experiments have revealed its functions in these areas, offering potential therapeutic targets for diseases such as diabetes-associated muscle atrophy and cancer [1,2,3,4].