Yin Xinbao, Xu Chuanshen, Zheng Xueping, Yuan Huiyang, Liu Ming, Qiu Yue, Chen Jun
Department of Urology, Qilu Hospital of Shandong University, Qingdao, Shandong 266035, P.R. China.
Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Oncol Rep. 2016 Sep;36(3):1535-41. doi: 10.3892/or.2016.4939. Epub 2016 Jul 15.
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.
转录调节因子SnoN（也称为Ski样原癌基因，SKIL）是Ski家族的成员，据报道它可响应转化生长因子-β（TGF-β）影响上皮-间质转化（EMT）。在本研究中，我们调查了SnoN在膀胱癌（BC）中的作用。与相邻的非癌组织相比，未在BC组织中检测到SnoN的差异表达。SnoN在TGF-β处理后上调，但对TGF-β信号通路没有影响，这可能是由于SnoN的SUMO化水平较低所致。催化SnoN SUMO化的TIF1γ在BC组织中下调。TIF1γ的过表达恢复了SnoN抑制TGF-β信号通路的能力。此外，在存在SnoN的情况下，TIF1γ抑制了TGF-β诱导的BC细胞EMT和侵袭。总体而言，我们的数据表明，SnoN以TIF1γ依赖的方式抑制TGF-β诱导BC细胞的EMT和侵袭，并可能作为治疗BC的一种新的治疗选择。
