Guan Hong-Jun, Li Xiao-Xia, Guo Yu-Peng, Dong Jing, Rong Sheng-Zhong, Niu Ying-Ying, Meng Li-Li, Zhao Fu-Yang, Fan Xing-Jun, Zhang Yue-Shun, Yang Yin-Dong, Nan Xi-Hao, Qi Bao-Lin
College of Public Health, Mudanjiang Medical University Mudanjiang, Heilongjiang, P. R. China.
Hongqi Hospital Affiliated to Mudanjiang Medical University Mudanjiang, Heilongjiang, P. R. China.
Int J Clin Exp Pathol. 2017 Nov 1;10(11):11326-11334. eCollection 2017.
It has been identified consequences of dysregulation of JAK-STAT signalling, particularly in regard to JAK-STAT signalling that has been shown to have roles in the oncogenesis of several cell types. SOCS3 protein, the negative regulatory protein of JAK-STAT signaling pathway, may also plays critical regulatory roles in cancer initiation and progression. SOCS3 promoter hypermethylation has often been identified in human cancers; however, the precise role of SOCS3 in bladder cancer is unclear.
The methylation status of the SOCS3 was analyzed in an age (±5 years) and sex-matched case-control study, including 112 bladder cancer cases and 118 normal controls, using the MassARRAY EpiTYPER system.
Methylation rate of JAK2, SOCS3 and STAT3 gene were shown to vary among different CpG island. The methylation rate of SOCS3 gene was also much higher in BCa than in normal control participants, but the methylation rate of JAK2, STAT3 gene weren't different in Bca and normal control participants.
Our study demonstrates that promoter hypermethylation of SOCS3 gene is associated with BCa and thus, may serve as an independent prognostic biomarker.
已确定JAK-STAT信号失调的后果，特别是在已显示在几种细胞类型的肿瘤发生中起作用的JAK-STAT信号方面。SOCS3蛋白是JAK-STAT信号通路的负调控蛋白，在癌症的发生和发展中也可能起关键的调控作用。SOCS3启动子高甲基化在人类癌症中经常被发现；然而，SOCS3在膀胱癌中的具体作用尚不清楚。
在一项年龄（±5岁）和性别匹配的病例对照研究中，使用MassARRAY EpiTYPER系统分析了112例膀胱癌病例和118例正常对照中SOCS3的甲基化状态。
JAK2、SOCS3和STAT3基因的甲基化率在不同的CpG岛之间有所不同。SOCS3基因的甲基化率在膀胱癌中也远高于正常对照参与者，但JAK2、STAT3基因的甲基化率在膀胱癌和正常对照参与者中没有差异。
我们的研究表明，SOCS3基因启动子高甲基化与膀胱癌相关，因此可能作为一种独立的预后生物标志物。
