标题：SnoN suppresses TGF--induced epithelial-mesenchymal transition and invasion of bladder cancer in a TIF1-dependent manner
作者：Yin, Xinbao; Xu, Chuanshen; Zheng, Xueping; Yuan, Huiyang; Liu, Ming; Qiu, Yue; Chen, Jun
作者机构：[Yin, Xinbao; Yuan, Huiyang; Liu, Ming; Qiu, Yue; Chen, Jun] Shandong Univ, Dept Urol, Qilu Hosp, 758 Hefei Rd, Qingdao 266035, Shandong, Peoples R Ch 更多
通讯作者：Chen, J;Chen, J
通讯作者地址：[Chen, J]Shandong Univ, Dept Urol, Qilu Hosp, 758 Hefei Rd, Qingdao 266035, Shandong, Peoples R China;[Chen, J]Qilu Hosp Shandong Univ, Dept Urol, Qin 更多
关键词：epithelial-mesenchymal transition; SnoN; TGF-; TIF1; bladder cancer;; cell invasion
摘要：The transcriptional regulator SnoN (also known as SKI-like proto-oncogene, SKIL), a member of the Ski family, has been reported to influence epithelial-mesenchymal transition (EMT) in response to TGF-. In the present study, we investigated the role of SnoN in bladder cancer (BC). Differential expression of SnoN was not detected in BC tissues compared with that noted in adjacent non-cancerous tissues. SnoN was upregulated in response to TGF- treatment, but had no effect on the TGF- pathway, which may be explained by the low level of SnoN SUMOylation. TIF1, which cata-lyzes the SUMOylation of SnoN, was downregulated in BC tissues. Overexpression of TIF1 restored the ability of SnoN to suppress the TGF- pathway. Furthermore, TGF--induced EMT and invasion of BC cells were suppressed by TIF1 in the presence of SnoN. Collectirely, our data suggest that SnoN suppresses TGF--induced EMT and invasion of BC cells in a TIF1-dependent manner and may serve as a novel therapeutic option for the treatment of BC.