Knockdown of FAT10 inhibits proliferation and growth in bladder cancer (8). FAT10 protein expression is upregulated in bladder cancer and increased expression of FAT10 is correlated with progression and poor prognosis of bladder

Epithelial to mesenchymal transition (EMT) serves important roles in tumor invasion, metastasis, formation of cancer initiating cells (CICs) and drug resistance. HLA-F adjacent transcript 10 (FAT10) has been proposed as an oncogene in bladder cancer. However, the functional contribution of FAT10 to EMT and the formation of CICs remains unclear in bladder cancer. The present study reports that FAT10 protein expression is upregulated in bladder cancer cell lines, and the overexpression of FAT10 promotes EMT and the formation of CICs in bladder cancer UMUC-3 cells. In addition, increased expression of FAT10 in tumor tissue was associated with shorter overall survival and progression free survival in Chinese patients with bladder cancer. Overexpression of FAT10 promotes cisplatin-resistant bladder cancer formation. These results indicated FAT10 may be a novel target for the treatment of bladder cancer.