SnoN suppresses TGF-β-induced epithelial-mesenchymal transition and invasion of bladder cancer in a TIF1γ-dependent manner.

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-β. 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-β treatment, but had no effect on the TGF-β pathway, which may be explained by the low level of SnoN SUMOylation. TIF1γ, which catalyzes the SUMOylation of SnoN, was downregulated in BC tissues. Overexpression of TIF1γ restored the ability of SnoN to suppress the TGF-β pathway. Furthermore, TGF-β-induced EMT and invasion of BC cells were suppressed by TIF1γ in the presence of SnoN. Collectirely, our data suggest that SnoN suppresses TGF-β‑induced EMT and invasion of BC cells in a TIF1γ‑dependent manner and may serve as a novel therapeutic option for the treatment of BC.