Slc35f2, a member of the solute carrier family, belongs to membrane-bound carrier proteins [2,5]. Although its exact physiological function is yet to be fully elucidated, it has been implicated in multiple biological processes related to cancer. It has been associated with pathways such as apoptosis, adhesion, and the p53 signaling pathway [4].

Knockdown of Slc35f2 in bladder cancer cells inhibits their proliferation, migration, and invasion, and promotes apoptosis. In nude mice, Slc35f2 knockdown significantly reduces tumorigenesis, suggesting its role in promoting bladder cancer progression [3]. In pancreatic cancer cells, it has been found that the Slc35f2-SYVN1-TRIM59 axis critically regulates ferroptosis by inhibiting endogenous p53. High expression of Slc35f2 is related to adverse survival outcomes in pancreatic cancer patients [1]. In HeLa cells, depletion of βTrCP1 or APC/CCdh1, which interact with Slc35f2 to promote its ubiquitination and degradation, accumulates Slc35f2 protein and promotes Slc35f2-mediated cell growth, migration, invasion, and colony formation ability, indicating their role in suppressing Slc35f2-mediated carcinogenesis [2,5].

In conclusion, Slc35f2 plays a significant role in cancer-related biological processes, especially in promoting the progression of cancers like bladder and pancreatic cancer. The findings from knockdown experiments in cell lines and in vivo models in nude mice contribute to understanding its role in cancer, suggesting that Slc35f2 could be a potential therapeutic target for treating these cancers [1,2,3,5].