Posttranslational protein modifications are known to be extensively involved in the cancer process, and a growing number of studies have revealed that the ubiquitin-like modifier FAT10 is directly involved in cancer development. FAT10 was found to be highly upregulated in various cancer types, such as glioma, hepatocellular carcinoma, breast cancer and gastrointestinal cancer. Protein FAT10ylation and interactions with FAT10 lead to the functional change of proteins, including proteasomal degradation, subcellular delocalization and stabilization, eventually having significant effects on cancer cell proliferation, invasion, metastasis and even tumorigenesis. In this review, we summarize the current knowledge on FAT10 and discuss its biological functions in the cancer process, as well as potential therapy strategies based on the FAT10 pathway.
Keywords: FAT10, FAT10ylation, cancer, substrate, ubiquitin-like, post-translational modificatioFAT10, post-translational modification
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