Slc2a5, also known as GLUT5, is the major fructose transporter in mammalian cells. It facilitates the uptake of fructose into cells, which is then phosphorylated by ketohexokinase to form fructose 1-phosphate, participating in the fructose metabolism pathway. This process is of significance in various biological aspects, such as nutrient absorption and cell survival [2,4].

CRISPR/Cas9-mediated inactivation of the Slc2a5 gene inhibited cancer cell proliferation, migration in vitro and metastases in vivo in several animal models, uncovering its importance in directing mitochondrial function for cancer cell motility [1]. In lung adenocarcinoma, depletion of Slc2a5 undermined cell proliferation and invasion, while overexpression enhanced these processes [5]. In childhood Philadelphia chromosome-positive acute lymphoblastic leukaemia, tyrosine kinase inhibitors repressed Slc2a5 expression, and fructose protected tumour cells from drug-induced cell death [3]. In tumor endothelial cells, inhibiting Slc2a5 attenuated dietary fructose-enhanced tumor angiogenesis [6].

In conclusion, Slc2a5 plays a crucial role in fructose-mediated processes. Gene-knockout and other loss-of-function models have revealed its significance in cancer-related processes, including metastasis, cell proliferation, and angiogenesis, providing potential therapeutic targets for cancer treatment.